Conquering Autoimmunity

Autoimmune Paleo Cookbook

If you have an autoimmune disease, recipes can often be hard to find and you are often told the huge amounts of things like chocolate and certain foods with too high of a fat content that you can and can't eat. This eBook gives recipes that anyone can prepare without too much trouble. Even if you don't like cooking, this book makes cooking easy and breaks it down into steps. Best of all, the recipes do not taste like healthy medicine recipes. These recipes are delicious foods that anyone would want to eat, even if they didn't have to eat healthy. This book contains over 70 amazing recipes for anyone with an autoimmune disorder. The book comes with two free ebooks: 7 Steps to Living Well With an Autoimmune Disorder and The Top 10 Autoimmune Diseases Checklist. If you want to learn about your autoimmune disease and the best and worst foods for you, this is the book for you!

Autoimmune Paleo Cookbook Summary


4.6 stars out of 11 votes

Contents: Ebook
Author: Samantha Miller
Price: $27.00

My Autoimmune Paleo Cookbook Review

Highly Recommended

The writer presents a well detailed summery of the major headings. As a professional in this field, I must say that the points shared in this manual are precise.

When compared to other ebooks and paper publications I have read, I consider this to be the bible for this topic. Get this and you will never regret the decision.

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The Autoimmunity Bible & Norton Protocol

A former autoimmunity (lupus) sufferer and alternative health specialist teaches you how to: Eradicate your autoimmune disease by addressing the single most important chemical imbalance on the cellular level as per groundbreaking new discoverie in the field. Avoid the traps that your adrenal glands set for you once you start using steroids. This reaction has been found to be responsible for autoimmunity flares in 81% of cases according to recent studies. If your disease caused a rash, now you can clear it out by getting rid of it's underlying triggers. Gain instant relief within 4 days to a week. Eliminate the debilitating life-altering pain in your joints and re-claim your life from the claws of autoimmunity. Eliminate the 2 overlooked obstacles that make any healing agent futile if your are suffering from an autoimmune disease. This is exactly why no drugs can cure autoimmune disorders. It's like pouring water into a hollow bucket. Reverse the processes that are most likely scavenging your kidneys. Read more here...

The Autoimmunity Bible & Norton Protocol Summary

Contents: Ebook
Author: Julia Liu
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Price: $37.00

Implications for Understanding the Mechanisms Inducing Autoimmunity

The mechanisms of terminating T-cell activation are important in preventing unwanted and unnecessary T-cell activity. Normally the majority of auto-reactive T cells are selected out and deleted through mechanisms of central tolerance in the thymus. Induction of autoimmunity must suggest that a protective mechanism has failed. Immune privileged tissues are not only regional immune sites that in the extreme terminate T-cell activity, but are also targets of autoimmune responses. Animal models of experimental autoimmune uveitis and encephalomyelitis have shown that immune privileged sites can also give insight into the regional tissue conditions that fail to terminate T-cell activity leading to autoimmunity. If the normal immune privileged microenvironment mediates the production of specific T-cell lym-phokines, then changes in the microenvironment also mean losing the ability to regulate the production of specific lymphokines by T cells activated in the ocular microenvironment. The...

The Bcl2 Family Proteins and Programmed Cell Death

Several Bcl-2 family members have been identified in humans, including both anti-apoptotic (cytoprotective) and pro-apoptotic (death-promoting) proteins (Green and Reed 1998 Kroemer and Reed 2000 Cory and Adams 2002 Danial and Korsmeyer 2004). The relative ratios of the pro- and anti-apoptotic proteins determine the ultimate sensitivity and resistance of cells to diverse death-inducing stimuli, including chemotherapeutic drugs, radiation, growth factor deprivation, loss of cell attachment to extracellular matrix, hypoxia, infection, and lysis by cytolytic T cells. Imbalances in their relative expression levels and activities are associated with major human diseases, characterized by either insufficient (cancer, autoimmunity) or excessive (AIDS, Alzheimer's disease) cell death.

Clarifying Mortality Rates

Attention to the quality of data regarding causes of death could provide insight into the mechanisms of preterm birth as well as the causes of fetal and early neonatal deaths. This approach would require clinicians to vigorously search for causes of death whenever a fetal or early neonatal death occurs. Petersson et al. (2004) found that 11.5 percent of fetal deaths that would have been characterized as unexplained were due to infections with parvovirus, cytomegalovirus, or enterovirus. Other possible causes that should be explored include thrombophilias (e.g., Factor V Leiden), fetomaternal hemorrhage, chorioamnionitis (which would include pathologic examination of the placenta and the umbilical cord), uterine anomalies, umbilical cord or placental anomalies, toxin or drug exposures, and maternal illness (e.g., diabetes, hypertension with or without preeclampsia, thyroid disease, and autoimmune diseases) (Gardosi et al., 2005). Because the most common condition associated with fetal...

Analysis of Known Posttranslational Modifications

Ubiquitin, a small protein of 76 amino acids, covalently attaches to proteins as monomers or lysine-linked chains. Proteins can become dynamically modified with ubiquitin by various enzymes, producing a number of different outcomes. Ubiquitin modifications are typically associated with protein degradation through targeting to proteasomes. However, ubiquitin has other cellular roles not associated with proteasomal degradation and it is also evident that the type of ubiquitin linkage to a protein may influence its fate. The defective regulation of ubiquitin has now been found in diseases ranging from developmental abnormalities and autoimmunity, to neurodegenerative diseases and cancer (Layfield et al. 2001 Weissman 2001).

Tgfpbased Immunotherapy For Cancer

For the sake of simplicity, we divide the etiology of autoimmune-like disease into thymic origin and or peripheral tissue origin (76,81,82). Many reports implicated TGF-P in the pathogenesis of autoimmune-like disease. Systemic administration of TGF-P suppressed the symptoms of experimental encephalomyelitis, whereas antibodies to TGF-P enhanced the disease (82,83). Mice null for TGF-P 1 developed autoimmune-like syndrome, including enhanced expression of MHC class I and II antigens, circulating systemic lupus erythema-tosus (SLE)-like IgG antibodies to nuclear antigens, pathogenic glomerular IgG deposits, and progressive infiltration of lymphocytes into multiple organs (84,85). Development of autoimmunity is normally resulted in selection processes in the thymus or through mechanisms that maintain tolerance in peripheral tissues. In the thymus, negative selection takes place at the CD4+ CD8+ double-positive stage (86). Because TGF-P regulates the maturation of these double-positive...

SHP1 Negatively Regulates Hematopoietic Cell Signaling

The motheaten phenotype is complex and these animals suffer from severe immune deficiency, autoimmune, and chronic inflammatory disease. Their death results primarily from pneumonitis due to accumulation of large numbers of macrophages and neu-trophils in the lung. The amassing of macrophages and neutrophils in the skin causes the hair and pigment loss that is the basis for their motheaten designation. Other defects in homozygous motheaten mice include hyperresponsiveness of BCR- and TCR-mediated signaling, elevated numbers of a subset of B cells that is associated with autoimmunity, and high concentrations of serum immunoglobulins. The motheaten mice have been invaluable for investigating the function and regulation of SHP-1 in leukocytes. Despite the pleiotropic effects of these mutations on immune function, most studies with motheaten mice have consistently shown that SHP-1 negatively regulates a variety of signal transduction pathways in cells of hematopoietic origin.

Regulatory CD4 T cells

Immunological tolerance is mediated by a number of mechanisms, including deletion of self-reactive B and T cells in the bone marrow and thymus respectively. In addition, it is now clear that a specialized population of T lymphocytes can actively suppress immune responses. These cells have been termed 'regulatory T cells' (Treg) and have a phenotype of CD4+ CD25+. Naturally occurring regulatory CD4+ T cells express high levels of CD25, the IL-2 receptor a-chain, and have been shown to suppress CD4 and CD8 T cells' responses to a range of stimuli, both in vitro and in vivo. In mice, CD4+ CD25+ regulatory T cells (Treg) are involved in maintenance of peripheral T-cell tolerance to self antigens and protection against autoimmunity. Human Treg appear to enrich within CD4+ CD25high T cells and constitute approximately 1-5 of peripheral blood CD4 lymphocytes. In vitro, Tregs are cytokine independent and require cell contact to mediate suppressive action. However, Tregs are able to induce...

The Different Types of TCell Responses

The differentiation of effector Th cell is separated into three general types according to the lymphokines produced and the effector immune response elicited (Table 2). The DTH-mediating effector T cells are the type 1 Th (Th1) cells. Th1 cells are characterized by their secretion of interferon-y (INF-y) and tumor necrosis factor (TNF). The type 2 Th (Th2) cells mediate B-cell growth and allergic immune responses. The characteristic lymphokines produced by Th2 cells are IL-4 and IL-10. A third type of Th (Th3) cell has only recently been characterized. They are the result of oral tolerance and possibly the effect of aqueous humor (fluid from the anterior chamber of the eye) factors on activated T cells. These Th3 cells produce transforming growth factor-P (TGF-P) and IL-4 or IL-10. They have the ability to suppress autoimmune diseases mediated by Th1 cells with a potential to also suppress Th2-mediated responses. The path of differentiation by the activated T cells is associated with...

The Need for Terminating Tcell Activity

It is reasonable to think that survival of the host relies on the activation of an effective immune response however, some immune responses can also jeopardize host survival. The need to terminate a T-cell response is necessary to maintain homeostasis. Here T-cell responses are terminated to prevent activation when there is no noxious pathogen, or when a noxious pathogen has been cleared. Termination of T-cell responses is necessary when there is a hyper-sensitivity response that permanently damages tissues and organs such as in the eye. There is also the desire to therapeutically terminate T-cell activity to treat autoimmune disease and transplant graft rejection. The mechanisms of terminating Th-cell activity are the means by which the adaptive immune response establishes homeostasis, self-tolerance, and immune privilege.

Future Development for Improving the Protein Quality in Infant Formula

With the advent of new methodology, the identification of milk proteins and their biological activity has received more attention. Indeed, we have recently reported that human milk contains proteins such as transforming growth factor (TGF)-p 43 , osteoprotegerin 44 and soluble CD14 45 , which are involved in immune homeostasis, innate responses to bacterial components and bone metabolism. TGF-p is a multifunctional polypeptide. It acts upon a variety of different cells to regulate their growth, differentiation and survival, and plays a crucial immunoregulatory function in mechanisms of tolerance and the prevention of disease and autoimmunity 46 . TGF-p is present in milk and may be activated by acidification or mild enzymatic treatment 47 , thus it is feasible that it is activated during intestinal transit to exert a biological effect in the intestinal epithelium of the host. Furthermore, since TGF-p is present in bovine milk, we considered that it may remain biologically active after...

Suppression of TCell Activity by Active Cell Death

The importance of Fas-mediated Th-cell death has been shown in mice that are defective in Fas or FasL. These mice suffer from autoimmune diseases, but display normal adaptive immune defenses to infectious pathogens and to immunizations with foreign antigens. Peripheral tolerance to autoantigens must be mediated in part through Fas-mediated apoptosis. The potential for repeated activation of autoreactive Th cells in the periphery could promote Fas-mediated apoptosis. The Fas-mediated apoptosis is also important in mediating immune homeostasis. Because activated Th cells up-regulate both Fas and FasL, it is possible that excessive numbers of activated Th cells could regulate the extent of their activity by mediating apoptosis among themselves. This may also be one of the mechanisms that terminates Th cell activity once a noxious pathogen has been cleared. Th cells that escape this regulation may go on to be memory Th cells.

The Mechanisms of Immunosuppression

Our increasing understanding of the mechanisms that terminate T-cell activity has led to potential therapeutic approaches to prevent and cure autoimmune disease and to treat other immune-mediated events such as transplant graft rejection (Table 6). The mechanisms of oral tolerance brings forth the potential to cure and prevent autoimmune disease through induction of Th3 cells (antigen-specific, TGF-P-producing, regulatory T cell). Oral tolerance can be considered as an immunization to autoantigen under conditions that favor development of Th3 cells over Th1 and Th2 development. To prevent transplant graft rejection, induction of active T-cell death through transfection of Fas ligand genes into transplanted tissues has been shown to promote allograft survival. Unfortunately, some FasL-expressing grafts undergo acute graft rejection because of Fas-mediated neutrophil degranulation and cytotoxicity. Other therapeutic approaches will most likely be developed to utilize the molecular...

Selected bibliography

This chapter describes the clinical presentations and mechanisms of the immunodeficiency diseases, focusing on those disorders that affect lymphocytes and complement. Defects in neutrophils are dealt with in Chapter 17. Immunodeficiency is either primary or secondary to other diseases, transplantation and various drugs. Although the first description of a patient with primary immunodeficiency (PID) was half a century ago, it is only in the last decade that significant advances have been made in our understanding of the molecular mechanisms. Over 50 separate genetic defects in lymphocytes or monocytes macrophages are now known, mostly very rare and presenting in infants and young children. However, the majority of patients with PID do not yet have a defined condition and are 'classified' as having 'common variable immunodeficiency - CVID'. This disorder, as well as many of the known single-gene defects causing PID, is associated with autoimmunity to blood cells and lymphoma, and...

Crossindex of references

121 , 124 , 138 , 142 , 157 , 170 , 172 , 174 , 194 , 195 , 214 , 216 , 218 , 233 , 238 , 239 , 240 , 244 , 250 , 251 , 252 , 261 , 263 , 306 , 305 , 307 , 315 , 322 , 323 , 346 , 348 , 378 , 379 , 389 , 412 , 418 , 419 , 431 , 440 , 441 , 452 , 461 , 464 , 470 , 479 , 496 , 497 , 498 , 499 , 513 , 555 , 557 , 560 , 568 , 572 , 589 , 590 , 596 , 602 , 613 , 617 , 628 , 641 , 643 , 647 , 649 , 650 , 654 , 655 , 657 , 661 , 664 , 682 , 690 , 701 , 703 , 716 , 717 , 718 , 719 , 720 , 731 , 741 , 745 , 748 , 750 , 751 , 752 , 757 , 759 , 763 , 774 , 778 , 779 , 794 , 804 , 809 , 814 , 815 , 832 , 833 , 835 , 840 , 852 , 855 , 862 , 864 , 876 , 878 , 879 , 886 , 887 , 897 , 938 , 954 , 962 , 963 , 964 , 965 , 966 , 967 , 968 , 971 , 973 , 974 , 975 , 976 , 993 , 998 , 1007 , 1013 , 1037 , 1044 , 1057 , 1086 , 1092 , 1093 , 1095 , 1097 , 1106 , 1114 , 1124 , 1149 , 1150 , 1165 , 1166 , 1167 , 1168 , 1169 , 1172 , 1174 , 1175 , 1176 , 1177 , 1178 , 1179 , 1181 , 1189 , 1190 , 1205 , 1217 ,...

Thrombotic thrombocytopenic purpura TTP

Provokes excessive release of von Willebrand factor. The metalloproteinase enzyme deficiency exists either as a hereditary condition or can be acquired as a consequence of autoimmune disease due to a specific IgG inhibitor of the enzyme. Many factors can precipitate both the congenital and acquired forms of TTP, including drugs, malignancy, bacterial infection, HIV and other viral infections. Pregnancy is the precipitating factor in 10-25 of cases (Chang and Kathula, 2002 Proia et al., 2002).

The red cell membrane and chemistry of blood group antigens

Membrane Blood Group Antigens

Customary to define an antigen as a substance that can stimulate an immune response (immunogenicity). Immune responses can be either positive or negative. Positive responses lead to the production of antibodies (humoral immunity) and or proliferation of immunocompetent cells (cellular immunity) that can bind and eliminate their stimulatory antigen. In negative responses, the cells that mediate humoral and cellular immune responses are rendered non-responsive. This state is described as acquired immunological tolerance and is important in preventing autoimmune disease, as well as in establishing the 'take' or acceptance of transplanted syngeneic and allogeneic tissues.

Conclusion Of Precelampsia

A. (1990). Myasthenia gravis presenting as weakness after magnesium administration. Muscle Nerve, 13(8), 708-12. Belfort, M.A. (1992). The effect of magnesium sulphate on blood flow velocity in the maternal retina in mild pre-eclampsia, a preliminary colour flow, Doppler study. Br. J. Obstet. Gynaecol., 99(8), 641-5. Belfort, M.A. and Moise, K.J., Jr. (1992). Effect of magnesium sulfate on maternal brain blood flow in preeclampsia a randomized, placebo-controlled study. Am. J. Obstet. Gynecol., 167(3), 661-6. Belfort, M.A. and Saade, G.R. (1993). Retinal vasospasm associated with visual disturbance in preeclampsia color flow Doppler findings. Am. J. Obstet. Gynecol., 169(3), 523-5.

Blepharophimosis syndrome

PLASTIC and ORBITAL SURGERY Myasthenia gravis The Tensilon test identifies whether a dose of intravenous Tensilon (edrophonium hydrochloride) transiently improves an observable weakness such as ptosis. However, a negative result does not rule out myasthenia gravis. Serum antibodies to acetylcholine receptors are detectable in a majority but not all patients.

Bone marrow failure and relationship between paroxysmal nocturnal haemoglobinuria and acquired aplastic anaemia AAA

PNH has an intimate link with AAA, for several reasons. As stated above, sometimes a patient with PNH becomes 'less haemolytic' and more pancytopenic and ultimately evolves to frank AAA. In terms of pathogenesis, it is believed that AAA is essentially an organ-specific autoimmune disease that is mediated by 'activated' cytotoxic (CD8+) T lymphocytes, which are able to inhibit haemopoietic stem cells. Recently, skewing of the T-cell repertoire indicating the presence of abnormally expanded T-cell clones has been observed also in PNH. Most importantly, intensive immunosuppressive treatment is standard of care in AAA, and a beneficial response to the same treatment can be obtained also in PNH (see below).

Conclusions And The Injury And Regeneration Hypothesis Of Prostate Carcinogenesis

A model has been proposed (3,4) that suggests that repeated bouts of injury to the prostate epithelium, presumably as a result of inflammation in response to unknown pathogens or autoimmune disease and or dietary factors, result in proliferation of epithelial cells that possess a phenotype intermediate between basal cells and mature luminal cells. These cells are hypothesized to be attempting tissue repair. This is supported by the finding that several proteins known to be involved in tissue repair, such as C-met (25) and hepatocyte activator inhibitor-1 (74), show elevated expression in focal atrophy. The model predicts that in a small subset of cells somatic genome alterations occur, such as such as cytosine hypermethylation within the CpG island of the GSTP1 gene and telomere shortening, that drive genetic instability and initiate high-grade PIN and prostate cancer formation. A classification system of focal atrophy lesions (17) was recently validated that should aid in further...

Differential diagnosis of primary and secondary antibody deficiency

Secondary antibody deficiency must be excluded, being relatively common nowadays with many patients being treated with immunosuppressive and cytotoxic drugs. A variety of anti-inflammatory and anticonvulsant drugs have been associated with low serum immunoglobulins, and nearly 10 of patients treated for vasculitis with combinations of cyclophosphamide and steroids develop hypogammaglobulinaemia. The increasing use of combination therapy for malignancy and anti-B lymphocyte therapy for autoimmune disease is likely to be associated with an increase in the numbers of patients with secondary antibody deficiency. The mechanism for this complication is not known but is likely to be complex and involve polymorphisms in enzymes that metabolize specific classes of drugs. Other causes of secondary antibody deficiency such as increased loss from the kidney (nephrotic syndrome) can be easily eliminated, but protein loss from the bowel may be more difficult to confirm, particularly if the serum...

Answers and Explanations

Myasthenia gravis is characterized by a decreased density of acetylcholine (ACh) receptors at the muscle end plate. An acetylcholinesterase (AChE) inhibitor blocks degradation of ACh in the neuromuscular junction, so levels at the muscle end plate remain high, partially compensating for the deficiency of receptors. 18. The answer is B V C 4 b (3) . Dopaminergic neurons and D2 receptors are deficient in people with Parkinson's disease. Schizophrenia involves increased levels of D2 receptors. Myasthenia gravis and curare poisoning involve the neuromuscular junction, which uses acetylcholine (ACh) as a neurotransmitter.

It is Easy to Categorize but Harder to Live with Intermediates or Ambiguity

2002, 2004 Lockshin and Zakeri, 2004a-c C.O. B. Facey and R.A. Lockshin, in preparation). This argument would be consistent with observations of others emphasizing the protective role of autophagy that inactivation of autophagy genes disrupts the formation of dauer larvae in Caenorhabditis (Melendez et al., 2003) the neonatal death of mice that lack Atg5, during the time that they must switch from placental nourishment to milk (Kuma et al., 2004) and the importance of autophagy in prolonging the life of cells deprived of growth factors (Boya et al., 2005 Lum et al., 2005). If such cells are not rescued, they die with a morphology typically described as autophagic cell death, with DNA fragmentation occurring very late if at all (Okada and Mak, 2004 Kroemer et al., 2005). One draws from this discussion the following arguments. First, apoptosis or programmed cell death is a very important and well-regulated process it is not the event once considered to be passive. Second, in an acute...

Introduction to Diabetes

There are two main types of diabetes. Type 1 diabetes, also known as insulin-dependent diabetes mellitus, is an autoimmune disorder associated with MHC genes (Campbell and Milner 1993). Type 2 diabetes, known as non-insulin-dependent diabetes mellitus, is a complex multifactorial disease. Type 2 diabetes accounts for 90 of the diabetic population, affects nearly 130 million people and is expected to reach epidemic proportions in the next 10 years (Zimmet and McCarthy 1995 Zimmet 1995). This dramatic increase in the prevalence of type 2 diabetes was predicted 10 years ago when urbanisation, industrialisation and western habits became increasingly widespread in developing countries. This means that type 2 diabetes is a truly global health problem. It is of high cost and suffering primarily owing to its long-term complications.

Detection of tumorassociated antigens

Although the identified antigens in the prostate cancer models are not truly tumor specific, the rationale for their use in cancer vaccines remains. The potential for generating autoimmunity is less ominous given that the prostate is relatively dispensable. Also, the normal tissue counterparts of many tumors express low levels of MHC class I, allowing a possible window in the therapeutic index, if a tissue-specific response can be elicited.80

Changes in disease

Animal studies (Jafarian-Tehrani & Sternberg, 1999) have suggested that the HPA axis response to stress may also be impaired in chronic stress, allowing a susceptibility to autoimmune diseases to emerge. The mechanism is unclear but similar observations in patients with atopic eczema (Buske-Kirschbaum et al., 1997) and rheumatoid disease (Gutierrez et al., 1999) have been recorded.

Timothy J Sullivan

Although many conditions can affect the orbit, the symptoms of orbital disease are relatively limited (Box 10.1) and most diseases are of structural, inflammatory, infectious, vascular, neoplastic or degenerative origin. A thorough history and systematic examination usually provides the astute clinician with a concise differential diagnosis and will guide appropriate further investigation in particular, the temporal sequence and speed of events is very important in suggesting the likely disease. A general medical history, a history of trauma or prior malignancy, and a family history of systemic diseases (for example, thyroid or other autoimmune diseases) are also very important.

Patient Associations

These groups typically focus primarily on one specific disease or type of disease process (e.g. inborn errors of metabolism, muscle disease, glycogen storage diseases, autoimmune diseases). Occasionally, they may serve as umbrella organizations for larger numbers of rare diseases, in order to achieve


Magnesium sulfate is a weak calcium channel blocker that regulates intracellular calcium flux through the N-methyl-D-aspartate receptor in neuronal tissue and may inhibit ischemic neuronal damage brought about by anion flux through this receptor (Altura and Altura, 1984). Parenterally administered magnesium results in systemic vasodilatation and improved cardiac output as well as cerebral vasodilatation distal to the middle cerebral artery. Retinal artery vasospasm has been reversed by magnesium sulfate infusion (Belfort, 1992 Belfort and Moise, 1992 Belfort et al., 1992). The myocardial effects of parenteral magnesium include slowing of the cardiac conduction times, and in high doses magnesium is significantly negatively inotropic (Arsenian, 1993). Intravenous magnesium sulfate reduces serum calcium levels possibly as a result of increased renal magnesium and calcium excretion (Arsenian, 1993). Falling serum calcium levels inhibits acetylcholine release at the motor endplate, the...


The specific mechanism of platelet autoimmunity remains unclear. Higher levels of platelet-bound IgG and complement are seen in HIV-related ITP than in classic ITP, and circulating immune complexes capable of binding normal platelets can be found in the serum. In contrast with classic ITP, the eluates of the platelet-associated immunoglobulins in HIV-associated ITP react against normal platelets in only a minority of patients. In HIV patients, unlike patients with classic ITP, platelet counts are not inversely related to platelet-bound IgG, although it is likely that the deposition of immune complexes leads to increased peripheral destruction of platelets by phagocytic cells. The nature of the immune complexes has been extensively studied. They lack HIV antigen and proviral DNA but contain anti-HIV gp120 and anti-antibodies directed against the anti-HIV antibodies. In some patients cross-reactivity of antibodies against HIV gp120 gp160 with platelet glycoprotein GPIIb IIIa has been...

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