Immune System Diseases

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Immune deficiency disorders, such as AIDS, chronic weakness syndrome, as well as cancer, and autoimmune diseases, have been a menace of modern medicine, not only because there is no known cure, but also because the modern medicine found no effective way to slow down the progress of such illnesses. 


During the last few years there has been a growing body of peer-reviewed publications reporting on the success of fetal precursor cell transplantation in the treatment of many cancers, both solid, and dispersed. So perhaps the scientific fact that fetal precursor cell transplantation is by far the most potent immuno-stimulant known to medicine today stops being one of the 'best kept secrets'.  Immune system testing is still not sufficiently sensitive to assess the degree of benefit of the immuno-stimulating effect of fetal precursor cell transplants.


Modern medicine has a very limited armamentarium of therapies for immune deficiencies. With exception of fetal precursor cell transplants there are no effective direct immuno-stimulants available for treatment.  Fetal precursor cell transplantation stimulates immune system spectacularly well, particularly one that is weakened for one reason or another. And that applies to even such deadly diseases of immune system as AIDS, and cancer, in which the immune system is malfunctioning as a result of an illness and a method of treatment used to combat it. 


It is therapeutically effective also against autoimmune diseases, apparently functioning as an immuno-modulator in a way that lacks a scientific explanation.


The survival of a live organism without a defense against harmful factors of the outer and inner world, whether living or non-living, is impossible. The defense mechanism that has developed since the inception of life millions of years ago is a complicated and highly organized system which protects the biologic existence of every living being. Contact with, and defense against, the environment are key properties of life. Intake and metabolism of life-sustaining matters are recognized as fundamental biological features, but the defense against damaging and life-threatening matters is on the same level of importance.


As sophisticated as the immune system is, it operates on a very simple basic principle. It distinguishes 'self' from 'non-self' and attacks 'non-self' with the ultimate goal of removing it from the body. Usually this works in our favor, such as when our body is attacked by pathogenic microbes. At other times it works against us, such as when our life depends on a transplanted organ: heart, liver or kidney, and our immune system attacks it as 'non-self' and causes its rejection. Sometimes the immune system fails to recognize even parts of our own body as 'self' and attacks them as 'non-self', and an autoimmune disease develops.


The immune system consists of four components:

1/ the epithelial surface, protecting the organism against outside world and the microbial world inside of our bodies, as there are more microbial cells in our body than of our own cells, and that is historically, or phylogenetically, the oldest part; 2/ the reticulo-histiocytary system, spread diffusely throughout our body, that developed next; 3/ thymo-lymphatic system, consisting of thymus gland, and  network of lymphatic vessels carrying lymph, which is filtered in lymphatic nodes, and 4/ spleen, which filters blood, among other functions, and these last two are the youngest parts.


Immune system defends body against microorganisms, and macromolecules recognized as ‘foreign’, by non-specific inborn, and associated with it specific acquired, or adaptive, immunity. Parts of microorganisms and ‘foreign’ macromolecules behave as ‘antigens’, and specific acquired immune system reacts to them by activation and multiplication of mono-specific T- and B-lymphocytes. Both B- and T-lymphocytes have receptors on their surface for detection of foreign antigens that specifically enable their activities, and production of cytokines, low-molecule soluble polypeptides, and their secretion into the surrounding extracellular space, that participate in elimination of the ‘non-self’ cells or macromolecules by non-specific mechanisms..


The lymphocytes are the most important cells of our defense system. More than a trillion of them are in the body at once, either circulating in the blood or on guard in the lymph nodes. There are two types of lymphocytes: T-cells and B-cells. Both are formed in bone marrow. B-cells mature in blood, while T-cells must pass through and mature in thymus gland. Thymus instructs the lymphocytes how to recognize 'non-self' and what to do when 'non-self' invades the body.


B-lymphocytes differentiate after stimulation by an antigen into plasma cells, which produce and secrete into body fluids antibodies, i.e. immunoglobulins IgA, IgD, IgE, IgG, IgM, that react with antigens that triggered their differentiation, neutralize or opsonize antigen, and activate complement system, i.e. humoral immunity. They do not enter live cells. Every B-lymphocyte is programmed to produce one specific antibody. This system has a memory. Once a B-cell produced an antibody against a specific foreign antigen, it remembers it forever. Thus each succeeding wave of the same infection, or the same antigen, is fought off with an increasing efficiency. This is the basis for immunization and explains why we fall victim to several childhood infectious diseases only once. The 'immunological memory' works sometimes in the opposite direction, i.e. in allergic conditions, ranging from hay fever to sudden death due to anaphylactic shock.


T-lymphocytes are the sentries of our body. When the ‘non-self’ antigen is recognized, they ‘sound an alarm’ and direct cooperation of different cells of immune system, including histiocytes, macrophages, etc., and various non-cellular components, i.e. complement, cytokines, etc., and directly attack somatic cells infected by virus, or that turned malignant, and cause a rejection of tissue transplants, i.e. cell immunity. T-cells are divided into T-helpers, responsible for co-activation of B-lymphocytes and thereby production of antibodies, supporters of function of NK-cells, and T-cytotoxic/ suppressors, responsible for uncovering and destruction of virus infected cells.


Any antigen is ‘remembered’ by T- and B-memory cells. From lymphoid precursor cells without any receptors, develops during their ‘upbringing period’ in thymus for T-cells, and in bone marrow for B-cells, a repertoire of about 108 of various types of lymphocytes, that are mono-specific, i.e. directed against one specific antigen. Such ‘virgin’ lymphocytes circulate in the body, between blood, peripheral lymphatic tissue, lymph, and blood again. When such ‘virgin’ lymphocyte meets ‘its’ antigen, usually within lymphatic tissues, it multiplies, passes through clonal selection and proliferation, and a large number of mono-specific daughter cells is produced. These daughter cells differentiate into required T-cells, or B-cells, which eventually eliminate antigen.


‘Virgin’ lymphocyte with receptors against own body tissues is eliminated in thymus, i.e. T-cells, or in bone marrow, i.e. B-cells, early enough after recognition of ‘its’ antigen. Such ‘clonal deletion’ creates in this way a ‘central immunological tolerance’. This recognition of difference between foreign antigens and antigens of own body is ‘learned’ by immune system at the moment of birth. All substances that come in contact with immune system at that moment are recognized for the rest of life as ‘own’ and all others that come in contact with immune system later on as ‘foreign’. If this recognition fails, an autoimmune disease develops.


Immune system cells are characterized by their own system of membrane antigens, which appear in cell membrane at certain stage of development, remain there for a certain period of time, or up until cell death. These membrane antigens are known as clusters of differentiation (CD). Some CD are located on both T- and B-lymphocytes, others are specific for some cells only.


The defense capabilities of immune system have a 'life profile'. After 'immuno-tolerance' of the embryonic and fetal stage of life, when the immune system is not functioning and the entire defense depends on the immune system of pregnant mother and placenta, the immune system gradually 'wakes up', until it reaches the optimal functioning level between 10 and 15 years of age. During puberty the immune system function gets depressed, the exact timing depends on the sex.


Afterward the immune system works at full capacity for the next 30 to 35 years. 

Between 40 and 50 years of age a regression period begins, when the function of immune system decreases relentlessly until a senile 'immuno-paralysis' period is reached when body becomes defenseless against malignancy and even the most banal infections.


Non-specific immunity is handled by

- dissolved defensive substances, i.e. lysozym;

- various complements;

- phagocytosis, carried out mostly by macrophages, developed from monocytes, attracted from blood to tissues where infectious agents are present by chemokines (chemotaxis); here phagocytes trigger via mediator release the inflammatory process, and ‘ingest’ pathogenic microorganisms and destroy them with lysozym, oxidants, i.e. H2O2, and oxygen radicals (O2-, OH-, 1O2), nitrogen oxide (NO), and ‘digest’ them by their lysosomal enzymes; phagocytosis being more effective when the surface of antigen is covered by IgM or IgG, or by complement C3b during the process of ‘opsonization’;

- pathogenic organisms, ‘opsonized’, or’non-opsonized’, trigger also ‘complement cascade’ whereby a membrane attacking complement complex is created which perforates wall of gram-negative bacteria and kills them;

- non-specific defense against mycobacteria and cancer cells is handled by ‘natural killer cells’(NK cells), that perforate membrane of target cell and cause its death by cytolysis;

- macrophages, developed from monocytes that either traveled to the respective tissue from blood or were fixed in the local tissue, i.e. Kupffer cells in sinuses of liver, lung alveoli, intestinal serosa, sinuses of spleen, lymphnodes, Langerhans cells of skin, synovial A-cells, brain microglia, endothel, etc., that belong to reticuloendothelial system (RES) or mononuclear-phagocytic system (MFS).


Acquired specific immunity through mono-specific effector T-cells requires that ‘modified’ antigen is presented to such T-cells by ‘professional’ antigen presenting cells, i.e. APC’s. The ‘modification’ means that antigen is built into a molecular capsule of individually specific proteins of MHC class I and II, in humans known also as HLA class I and II. In lymphatic tissue residing virus-infected dendritic cells serve usually as APC’s. For presentation of antigen by APC a binding between an intracellular adhesive molecule (ICAM) on the surface of APC and a lymphocyte function associated antigen 1 (LFA-1) on the surface of T-cell is necessary. When T-cell approaches APC this binding becomes stronger and T-cell is activated by a double signal consisting of:

  • recognition of antigen, bound to MHC-I or –II, by the T-cell receptor with co-receptor, i.e. CD8 in cytotoxic T-cells, CD4 in T-helpers, and
  • co-stimulatory signal, i.e. binding of protein B7 (on APC) to protein CD28 of T-cell.


When antigen is bound without co-stimulatory signal, for example in liver where there are usually no APC’s, T-cell is actually inactivated, i.e. becomes anergic. This is known as ‘peripheral immunotolerance’.


Cytotoxic T-cells develop from ‘virgin’ CD8-T-cells after presentation of antigen associated with MHC-I, during which act MHC-I accepts its antigen mainly from cytosol of APC (antigens are viruses, or cytosol proteins), and for that reason it is called ‘endogenous presentation of antigen’. Cytotoxic T-cells recognize then by its CD8 associated receptor the respective MHC-I bound antigen on virus-infected cells, cancer cells, or cells of transplanted organs, and kill those cells.


‘Virgin’ helper CD4-T-cells change after the presentation of antigen (phagocytized bacteria or protein of viral capsules, i.e. ‘exogenous antigen presentation’) associated with MHC-II into immature effector T-cells (THO). The THO cells develop by differentiate into either inflammatory T-helpers (TH1), which activate macrophages, or T-helpers of 2nd type (TH2) necessary for B-cell activation.


Specific humoral immunity is dependent on B-cells.


Disorders of non-specific immunity can be due to

  • defects of complement system, i.e. infections by extracellular microorganisms, mainly neisserias,
  • defects of NK cells, i.e. infections by intracellular organisms, mainly listeria, or herpetic viruses,
  • mannose binding protein,
  • disturbances of phagocytosis involving various types of cells, or just functional defects, such as: leukocyte adhesion defect (LAD), syndrome of ‘lazy leukocytes’ with slowed down migration, chronic granulomatous disease with lack of oxidant production, Chediak-Higashi syndrome with disrupted fusion of phagosomes and lysosomes.


Disorders of humoral immunity can be due to defects of maturation, function or activation of B-cells. Without antibodies the organism is helpless especially against microorganisms causing suppuration, because without opsonization their polysaccharide capsule blocks phagocytosis. Here is a partial list:

  • selective lack of IgG with insufficient protection of mucosa causes recurrent respiratory and GI infections and predilection to allergies,
  • agammaglobulinemia where defect of Bruton’s tyrosinkinase interferes with maturation of B-cells,
  • syndrome of higher IgM level characterized by concurrent lowered concentration of IgA and IgG,
  • variable defect of immunity with inadequate B-cell stimulation by T-cells.


Defects of cell-mediated immunity occur

  • in thymus aplasia, known as DiGeorge syndrome,
  • in combination with defects of humoral immunity, covering the whole spectrum of diseases from defects of stem cell differentiation, i.e. reticular dysgenesis, through defective HLA production, i.e. syndrome of naked lymphocytes, to a very serious combined B- and T-cell insufficiency, i.e. severe combined immunodeficiency disease, SCID, caused by a lack of adenosinedeaminase or purinnucleotidephosphorylase.


For direct immunostimulation fetal precursor cell transplantation of mesenchyme, thymus, spleen, liver, adrenal cortex, mesenterial lymphnode, intestine, is recommended, with an addition of lung when respiratory system defense is at stake, or skin, when immune protection of skin is necessary.


AIDS is caused by HIV-1 or HIV-2 viruses. Viruses attack, besides CD8 cells, predominantly CD4 TH-cells, in which ssRNA is transcribed by virion reverse transcriptase into cDNA, until it is as double chain dsDNA (provirus) placed into the genom of host cell during the latent stage. Between the initial viremia with high level of antigen p24 and production of IgM , and ARC with renewed viremia, without any IgM, many years can pass, during which time proviruses survive in small numbers, such as 106, of inactive CD4-cells mostly in lymphnodes. Activation of CD4 cell, at the beginning of infection and in the late stage, triggers virus expression. Even non-infected CD4 cells die so that in the late stage there is critical lack of CD4 T-cells. Changes of cytokine concentration cause a major elimination of TH1 and cytotoxic cells. The organism is now exposed with growing helplesness to otherwise unimportant minor infections, i.e. by fungi, and rare cancers, i.e. Kaposi sarcoma, lymphomas.


A case history of AIDS patient treated by cell transplantation is the sole published information about a U.S. clinical trial that began in New York after Prof.Dr. Schmid was approached in September 1987 and then visited on November 3, 1987, in the State Pediatric Hospital in Aschaffenburg, where he was a director, by Mr. Ed Kramer and Dr. Kohn, the organizers of the project. Approximately 30 patients were treated, in accordance with the protocol in possession of the author, but the project was stopped because of a lack of funds. The patient described in this publication continued to be treated for free as all expenses were paid for by the German Association for Cell Therapy and German manufacturers.


A 39 years old female from Houston, Texas, developed in 1965, at the age of 17, Hodgkin’s disease. After 13 surgeries and chemotherapy was since 1971 relatively well. In Januray 1986 developed an acute lymphadenitis treated by antibiotics and I&D. In April 1987 a pulmonary aspergillosis was diagnosed, followed by a diagnosis of AIDS Related Complex, with lymphocyte count of 2200/mm2, and a weight drop from 144 to 126 lb. On 5/25/87 she received cell transplants of thymus, mesenchyme, liver, spleen, skin. One week later her lymphocyte count increased, the first monocytes have appeared since about 8 months. The patient was feeling better, her appetite improved. In October 1987 an implantation of two cell transplants was carried out. WBC had remained normal, lymphocytes rose from 15 to 50%, CD8 cell count rose, CD4 cell count decreased, so that CD4/CD8 ratio improved from 0.60 to 0.88.


Then there was a treatment interruption, and the condition of the patient dramatically worsened. On May 25, 1988 CD4/CD9 ratio was 0.27. After the patient received cell transplantation of mesenchyme, liver, spleen, thymus, skin, placenta, in July 1988 the CD4/CD8 ratio went up to 0.40, CD4 T-cells rose from 10% to 24% but also CD8 T-cells from 34% to 63%, the patient was feeling much better and the immune system weakness was diminished. Here is where the report ends. VI.BIBLIOGRAPHY [287]


At one of the meetings of the International Society of Cell Therapy the conclusion of this case history was given. After 2 ½ years of ‘underground’ treatment the immune deficiency appeared again and the patient had to get urgently another cell transplantation. At that point U.S. Customs stopped twice in a row the free shipment of cell therapeutica from Germany and by the time the third shipment arrived the patient was dead.


A 24 years old male homosexual, with a history of mononucleosis 4 years before this report, and gonorrhea and cytomegalovirus infection 2 years later, developed two years later a severe herpes zoster. During the examination a hepatosplenomegaly, inguinal, axillary, cervical lymphadenopathy, recurrent bronchial infections, and positive HIV tests, were found. IgG was increased and IgA decreased, CD4/CD8 ratio was 0.34. Cell transplantation with mesenchyme was begun and repeated four times at weeks 2 – 4 – 8- 16 –24. Splenomegaly subsided, immunoglobulins were within normal limits. Six months after the last treatment the patient was well and working. VI.BIBLIOGRAPHY [311]


Therapeutic protocol of treatment of AIDS requires an avoidance of re-infection, a follow-up every 4 – 6 weeks for immune system function evaluation, and continuous repetition of cell transplantation whenever the laboratory tests of immune system show that the HIV virus is prevailing again. Any delays in the cell transplantation treatment are very risky. When the immune system is at the point of shutdown, the fetal cell transplantation must be done as an emergency, or there may be no response. Even patients with ARC-AIDS related complex, with 500 CD4 cells/ml, or those with fully developed AIDS, with 200 CD4 cells/ ml, can reach their normal lifespan, if compliant, and treated by fetal precursor cell transplantation as the therapeutic protocol calls for.


The clinical picture of immune system deficiencies is characteristic by recurrent, prolonged, often very serious and eventually life-threatening infections, and certain cancers. They are classified into 5 groups:


Combined deficit of lymphocytes:

- X-linked severe combined immunodeficiency(SCID) with incidence 1:50000 to 1:75000, defect of both T- and B-cells, with low B-cell count and no T-cells, and defect of alpha-chain of IL-2 produced by T-cells, causes a severe disorder of both cell and humoral immunity and thereby extreme sensitivity to pathogenic organisms, resulting in candidiasis, chronic otitis media, diarrhea, and sepsis. Treatment has been by bone marrow transplant;

- deficit of adenosinedeaminase, AR disorder, a purine enzymopathy, leads to accumulation of toxic metabolites damaging T- and B-cells, with pronounced lymphopenia, rachitic rosary on ribs, normal uric acid in urine;

- deficit of purine nucleosidephosphorylase, AR disorder, a purine enzymopathy leads to an accumulation of toxic metabolites damaging T- and B-cells, with lowered level of uric acid in urine;

- defect of class II HLA-antigens, or syndrome of naked lymphocytes, AR disorder, causes moderate to severe degree of immunodeficiency and thereby serious bacterial infections; there is always a predominance of T-suppressor cells, while normally the ratio of T-helpers to T-suppressors is 2:1, low level of immunoglobulins, low specific antibody production;

- reticular dysgenesis, AR disorder;

- Omen syndrome, with immunodeficiency leading to serious infections, and severe erythrodermia, hepatosplenomegaly, lymphadenopathy, continuous diarrhea, persistent leukocytosis with pronounced eosinophilia;

- immunodeficiency with hyper-IgM syndrome, XR disorder, causing a failure of interaction of T- and B-cells, responsible for recurrent pyogenic infections, particularly of biliary system, that causes liver damage, with increased levels of IgM, but very low levels of all other immunoglobulins, and persistent neutropenia.

- DiGeorge syndrome, AR disorder, with multiple anomalies of structures of 3rd and 4th pharyngeal pouch, i.e. congenital aplasia of thymus, congenital hypothyreosis combined with aplasia of parathyreoid glands, heart malformations, particularly conus arteriosus, variable immunodeficiency up to a total absence of T-cells.


Antibody defects:

- Bruton’s X-linked agamaglobulinemia, the first immunodeficiency discovered, with absent B-cells and plasma cells, and thereby decreased levels of all immunoglobulins, normal level of precursors stem cells in bone marrow, at the end of the first 6 months of life repeated bacterial infections, i.e. pneumonia, meningitis, appear, while the sensitivity toward viral infections is not increased, with exception of hepatitis and enteroviroses;

- deficit of heavy chain of immunoglobulins, AR disorder, cause IgG deficit, and thereby repeated pyogenic infections;

- selective IgA deficit is the most frequent of all immunodeficiency disorders, deficit of IgA is present despite a normal B-cell count, causing recurrent sino-bronchial infections, gastrointestinal diseases, autoimmune diseases, allergies, and malignant diseases.


Other typical syndromes:

- Wiskott-Aldrich syndrome, XR disorder;

- ataxia-teleangiectasia, AR disorder, see also in the chapter ‘Genetic diseases’;

- Bloom syndrome, see also in the chapter ‘Genetic diseases’;

- Hyper-IgE syndrome.


Lymphocyte malfunction:

- X-linked proliferative syndrome;

- Chronic granulomatous disease;

- Leukocyte adhesion deficit;

- Chediak-Higashi syndrome.


Complement System Malfunction

Therapy by bone marrow transplantation from HLA-identical sibling is of great benefit, but it has to be carried out before irreversible damage to the organism due to frequent infections took place. There is much less risk with graft vs. host disease, etc., when fetal precursor cell transplantation of liver, spleen, thymus, mesenchyme, adrenal cortex, intestine, is used.


CASE HISTORY:


The patient worked with the author as an anesthesiologist during the surgical courses that the author used to teach in a major Italian city 3 - 4 times a year from 1989 till 1993. He was an excellent anesthesiologist, very successful in his private practice, vivacious, and a good companion, too. During various social outings he showed great interest in and learned about our work in the field of fetal cell transplantation. In 1992 he ‘disappeared’ and the writer did not see him again until early 1994, when he desperately seeked a medical help.

V.D., born 1951, a white male, developed a flu in early 1992, from which he could not recover. He was continuously fatigued, more so that he ever experienced, and even prolonged sleep did not refresh him. He had muscle pains, constant headaches, and frequent sore throats. While before he could work 12 hours every day, give anesthesia simultaneously in two adjacent operating rooms, now he could not finish a single anesthesia case a day. Gradually the fatigue became so severe that he became convinced that he ‘is going to die, particularly since no medical professional that he consulted could help him’.

He was examined by every professor of internal medicine of reputation in Italy, every imaginable clinical test was carried out, all with negative results, and no one could establish a diagnosis, with the exception of some remarks such as ‘that must be some form of depression or psychoneurosis’. In reality everyone who knew this patient well, and the patient himself, were of the opinion that any psychiatric disease is out of question. The sole objective fact that could have contributed to this illness was a ‘burn-out’ due to long hours of stressful work every day, since his services were in great demand, as he was an excellent anesthesiologist indeed.

The patient took various antidepressants, as advised, but without any effect.

Eventually in 1993 he was referred to a U.K. physician, who - with his consulting team - made a diagnosis of chronic fatigue syndrome, even though all tests were again negative.

The treatment consisted of detoxification: intake of copious amount of distilled water, vegetarian diet, mostly in the form of raw fruits and vegetables, ecologically clean, mega doses of vitamins and minerals, in particular of Niacin, to force salivation.

The patient began to feel better, but his ability to work continued to be minimal. He could do no more than one anesthesia case a day, following which he was completely exhausted. The absence of sexual performance ruined his marriage. His social life was non-existent.

When he met the author again in 1994 he asked if he could not be helped by fetal cell transplantation.

The patient arrived on April 4, 1994, at Moscow.

A complete physical examination was done, which was negative, as always before. Among various laboratory tests that we carried out a complete blood count, peripheral blood smear, sedimentation rate, total T-cell count, CD4+ count, CD8+ count, serum immunoglobulin electrophoresis, Candida skin test, were all negative. But we finally succeded where all predecessors failed during the past two years when we found an objective proof of an immune system deficiency: lymphocyte proliferative response test to mitogen, and in vitro phagocytosis assays, were both significantly abnormal.

On April 7, 1994, a cell transplantation of adrenal cortex, liver, mesenterial lymphnodes, spleen, thymus, hypothalamus, intestine, mesenchyme, was carried out. The post-treatment course was uneventful.

The patient was delighted with the result of cell transplantation. Within 6 weeks he was able to work 8 hours a day without any difficulty, and could do even more, but wisely preferred not to. His social and sexual appetite returned to normal.

Unfortunately he could not find a single laboratory in Italy that could do lymphocyte proliferative response test to mitogens and in vitro phagocytosis assay, that would have enhanced our follow-up data, and did not wish to return to Moscow ‘unless he would be in serious trouble again’ and that never happened after our treatment.

He waited until we set up a clinical base in Germany and in March 1999 the patient received BCRO fetal precursor cell transplantation of liver, adrenal cortex, thymus, spleen, mesenchyme, mesenterial lymphnodes, testis, by the autor at a clinic in Germany. The post-transplantation course was uneventful.

The patient feels that he is perfectly healthy today. But he continues to watch his nutrition, and fluid intake.

It is to a great degree thanks to him that we were able to start to offer cell transplantation in Italy.

The patient underwent his next fetal precursor cell transplantation in November 2003 as treatment of aging disease.



Clinical protocol for fetal precursor cell transplantation treatment of a patient with immune system disorders

A proper preparation of the patient for fetal precursor cell transplantation is mandatory. A patient has to be brought into as good a clinical condition as possible by standard therapeutic means, e.g. to carry out fetal cell transplantation while the patient is in the condition of insufficiently treated infection, with all the metabolic consequences, is probably minimally effective and should be done only as a last resort. Patient must be detoxified, which means in particular the treatment of the gastrointestinal, respiratory and urinary tract and skin infections & related diseases by antibiotics, etc.


Parameters to be followed in patients before and after fetal precursor cell xeno-transplantation, and the frequency:


- Basic: once a month or as often as clinically necessary

i/ complete blood count with differential, and platelet count

ii/ peripheral blood smear

iii/ total T-cell count

iv/ serum IgG, IgM, IgA, (and IgE, if necessary)

v/ iso-agglutinin titers: anti-A and/or anti-B to evaluate IgM function

vi/ pre-existing antibody titers after immunization against polio or rubella virus, and against tetanus, diphtheria - to evaluate IgG function

vii/ sedimentation rate

viii/ x-rays of infested organ(s)

ix/ bacterial culture(s) from the infected organ(s)

x/ clinical status of ongoing infectious disease(s) process(es)

xi/ x-rays of chest, also to measure the size of thymus

xii/ delayed hypersensitivity skin tests: Trichophyton, mumps, Candida, fluid tetanus toxoid and if necessary, to carry out once a month, or as often as clinically indicated:

xiii/ total white blood cell count

xiv/ nitroblue tetrazolium dye reduction test (NBT)

xv / total serum complement activity (CH50)

xvi/ serum C3 and C4 levels


- Special, to be carried out if clinically necessary:

i/ total B-cell count once a month

ii/ T-subsets counts: T-helpers/inducers (anti-CD4 antibody),

T-suppressors/cytotoxic cells (anti-CD8 monoclonal antibody),

CD4/CD8 ratio, NK (anti-CD16 monoclonal antibody) once a month

iii/ antibody response to vaccines: tetanus toxoid, typhoid (for protein

antigen response), pneumococcus, unconjugated H. influenzae (for

polysacharide antigen response) as often as needed

iv/ IgG subclass levels as often as needed

v/ lateral x-rays of pharynx: tonsills, adenoids size

vi/ lymphocyte proliferative response test to mitogens, known-to-patient-

antigens, irradiated allogeneic white blood cells, (include lymphokines,

IFN and IL-2 production as clinically required) as often as necessary,


and include the following if clinically necessary as often as needed:

vii/ cell movement by Rebuck skin window

viii/ in vitro chemotactic essay

ix/ in vitro phagocytosis assay (latex particles, bacteria)

x/ intracellular microbial killing assay

xi/ complement and inhibitor assays

xii/ classical and alternative complement activity essays

Frequency of office visits: 4 weeks and 48 hours before fetal precursor cell xenotransplantation, 24 hours and then once a week for the first month after fetal precursor cell xeno-transplantation, and once a month thereafter.

Repeated fetal precursor cell transplantation to be carried as often as clinical course requires to maintain the function of all components of immune system at a normal or near-normal level.


For AIDS treatment the fetal precursor cell transplantation has to be repeated as often as every 6 weeks depending upon the clinical course of the disease(s).


CASE HISTORY:


Author was introduced to S.S., born 1942, a black male, a top man in the hierarchy of the U.S. Baptist Church, at a political/social function, in 1991, by a colleague Dr. A. J., and a mutual acquaintance Mr. C. C.

In May 1993 Mr. C.C. called the author, asking whether we could treat AIDS, and FAX-ed us a medical summary of S.S.

S.S. noticed in early 1992 a gradual development of weakness, malaise, diarrhea, weight loss, and overall wasting, which made it increasingly difficult for him to go through the preaching sermon. In February 1993 a diagnosis of AIDS was established. At the same time a diagnosis of syphilis was made, and an immediate treatment by depot Penicillin was carried out. As we did not receive an official medical summary from patient’s physician, we did not know what type of treatment of AIDS was tried. The patient wished to save his life but his doctors did not agree that he should seek treatment elsewhere.

The patient arrived in Moscow on July 18, 1993, and upon admission to the hospital was found to be in a near moribund state. He was emaciated, dehydrated, toxic, with a fever of nearly 104 F, with a low blood pressure, tachycardia. There was a right upper lobe pneumonia on the admission chest x-ray. Immediately an aggressive anti-shock treatment was instituted, including i.v. broad-spectrum antibiotics.

Important laboratory findings on hospital admission: Complete blood count showed minor leukocytosis, with a lymphopenia. Total T-cell count was less than 200/µliter. CD4 count was 0, so that CD4/CD8 ratio was 0 as well. Serum immunoglobulin electrophoresis showed increased IgG, and IgA. Culture and Sensitivity of sputum showed Pneumococcus.

The intensive anti-shock therapy was succesful. As the patient arrived at Moscow in a nearly terminal state, which is normally a contraindication for cell transplantation, a deep professional discussion ensued about carrying out the planned treatment.

Eventually on July 26, 1993, fetal precursor transplantation of thymus, liver, adrenal cortex, spleen, mesenterial lymphnodes, mesenchyme, intestine, was carried out. The post-treatment course was uneventful and patient was able to fly back to U.S. on July 30, 1993.

Within 4 weeks of the treatment the patient began a preaching tour through U.S. baptist churches, openly admitting his past transgressions, that caused his illness, declaring that “God’s miracle” in Moscow saved his life, and that he will not sin anymore.

On August 30, 1993, his complete blood count and total lymphocyte count were within normal limits. Patient was clinically in a complete remission.

Our team was at Sansum Medical Research Foundation, Santa Barbara, Calif., from July 31 until August 6, 1993, to treat 24 U.S. insulin-dependent diabetics with retinopathy and nephropathy, an event widely announced by U.S. media as “Russian rabbit cells treating U.S. diabetics”. During this time we attempted to visit with the patient, but could not reach him even via his private phone number, that he gave the author in Moscow. Finally we spoke to a man who claimed to be his physician. The author tried to impress upon him that our/his patient needs a very close follow-up, a continuous supportive treatment as per our treatment protocol, and repeated “minor” cell transplantations every 4 - 6 -8 weeks in accordance with the results of laboratory testing of the immune system function.

Despite the best efforts of the patient’s friends who arranged his treatment with our team in Moscow we were not able to continue our treatment whether directly or by sending fetal precursor cell transplants to the patient to be implanted by his U.S. physicians.

S.S. died sometimes in February 1994 allegedly of the lymphoma of the brain.


CASE HISTORY:


In 1980 a two years’ old boy with Down syndrome was brought from California to the State Pediatric Hospital in Aschaffenburg, Germany, where Prof.Dr. F. Schmid was a director. The complex therapeutic protocol for Down syndrome was begun, which included cell transplantations. The next cell transplantation was carried out in California.

In 1981 the patient was brought to Aschaffenburg again for the 3rd cell transplantation, this time accompanied not only by parents but also grandparents. The family was pleased with the improvement of symptoms of Down syndrome. After grandson’s third cell transplantation was carried out, the grandfather approached F. Schmid and asked for an examination, fully aware that he is a pediatrician.

55 years’ old grandfather was a high level manager at film studios. He complained of deepening malaise, lasting for ~5 years, which had lowered noticeably his capacity to work and enjoy life on many fronts. During those ~5 years he suffered from frequently recurring attacks of bronchitis and pneumonia, losing many days from work, and his physicians could do nothing to improve the situation.

Grandfather received cell transplantation for revitalization (liver, testes, placenta), stimulation of immune system (thymus), and support of the organs most abused by stress (hypothalamus, adrenal cortex).

In 1982 grandparents brought their grandson back to Prof.Dr. Schmid for another cell transplantation treatment. Grandfather was beaming because during the last 12 months he had had no bronchitis nor pneumonia, and did not lose a single day from work, which made his ‘superboss’ extremely happy.

The grandfather asked F. Schmid if he would be so kind to examine his wife as well.

The 50 years old grandmother, looking older than her age, appeared chronically ill. Her fingers were deformed, the joints of hands were swollen. She was obviously depressed when complained about pain, inability to hold a cup of coffee in her hands, or carry many household duties. She barely recovered from one infection when she caught the next one again. Her circulation was inadequate, she had low blood pressure, after being up for two hours she had to lie down again.

Her treatment consisted of nutritional advice, digestive enzymes, and cell transplantation for revitalization (liver, ovaries, placenta, spleen), for support of blood circulation and organs abused by stress (heart muscle, diencephalon, adrenal cortex, medulla), for immune system stimulation (thymus, mesenchyme), and for arthritis (cartilage).

In 1983 the grandson and grandparents were back in Aschaffenburg for another treatment. In Prof .Dr. Schmid’s office the grandmother was ‘playing piano in the air’ with her fingers to show off that her arthritis was gone. Her infections did not stop but were much less frequent, and blood circulation was still somewhat weak.

In 1985 F. Schmid received a letter from the grandmother. She was doing relatively well, her blood circulation was not too bad, but her infections were coming on again, and lasted for along time. She was very disturbed about her positive test for AIDS, in particular since she could not comprehend how she could have acquired such an illness.

Both she and her husband began to follow therapeutic protocol for AIDS, including frequent cell transplantation to support immune system. Three years later the immune system was back to normal and AIDS test became negative.