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Specific protein, thermostable alpha-globulin, was found with the use of immunochemical analysis in carbon eluents after hemosorption in patients with autoimmune diseases. It is suggested that positive clinical effect of hemosorption might be determined by sorption of thermostable alpha-globulin from the patients' blood.
Lymphocyte homeostasis is achieved by a balance between the production and death of lymphocytes. In particular, T lymphocytes differentiate and mature in the thymus and are released into the peripheral circulation, where they can travel to sites of encounter with antigen. Once in the circulation, T lymphocytes have varying life spans depending on whether they remain resting, become activated by antigen and replicate, or they become memory cells. The regulation of lymphocyte fate, especially the induction of programmed cell death, or apoptosis, has become a focus of intense molecular research, and much has been learned. In particular, the Fas receptor and other members of the tumor necrosis factor receptors, as well as their respective ligands, have emerged as key regulators of T lymphocyte apoptosis. We are studying genetic abnormalities of this death pathway, which we have found to underlie the human disease, autoimmune lymphoproliferative syndrome (ALPS). The study of ALPS has revealed that inhibiting the death of lymphocytes can lead to autoimmune consequences. Also, the homeostasis of T lymphocytes can be powerfully affected by viruses and other infectious agents. In particular, the human immunodeficiency virus can cause the attrition of CD4+ T lymphocytes by inducing the premature death of such cells. We are studying the molecular mechanism by which the HIV causes CD4+ T cell destruction.
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INTRODUCTION: The toxic myopathy caused by statins (HMG-CoA reductase inhibitors) is well established. Recent reports add to these effects systemic immune diseases including systemic lupus erythematosus, vasculitis, polymyositis or dermatomyositis. EXEGESIS: We report a case of dermatomyositis in a 69-year-old patient treated with pravastatin [Elisor]. She presented with typical features of dermatomyositis 2 years after she started a treatment with pravastatin. The treatment was discontinued and she slowly improved, with a transient dermocorticosteroid treatment. Eight other patients with dermatomyositis and chronic treatment with HMG-CoA reductase inhibitors are reported in the literature. All of them presented with classical features of dermatomyositis. The discontinuation of the treatment was followed by spontaneous clinical and biological improvement in 3/9 patients. The other patients received high doses of corticosteroids and improved, except one patient who died of respiratory failure (pulmonary fibrosis) despite the adjunction of oral cyclophosphamide [Endoxan]. In these patients, dermatomyositis can be considered as a severe adverse reaction to HMG-CoA reductase inhibitors although a distinct casual link cannot be definitely established. CONCLUSION: The increasing prescription of statins has led to the parallel increment of reported side-effects, where autoimmune diseases are now described. Among them, our case of dermatomyositis in a patient receiving pravastatin adds to the eight reported cases in the literature and highlights the potential role of statins as triggers of immune systemic diseases.
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The immune system has a complex and dynamic relationship with the nervous system, both in health and disease. The immune system surveys the central and peripheral nervous systems, becoming activated in response to foreign substances, infectious particles or neoplasms. Conversely, the nervous system modulates immune system function both through the neuroendocrine axis and through vagus nerve efferents. In disease states, this dynamic relationship is perturbed, resulting in neuropsychiatric diseases. In this manuscript, we will summarize fundamental principles of the immune system and its interaction with the nervous system. We will describe the critical components of the adaptive and innate branches of the immune system and will describe important effectors and signalling pathways in each. By understanding the principles of the immune system and how these principles relate to nervous system function, the reader will be prepared to interpret subsequent manuscripts in this issue.
The tissue damage caused by virus infection has been traditionally explained by the ability of viruses to multiply in cells and thereby injure or destroy them. Recent evidence suggests, however, that lesions may also be caused by the host's immune response to viral antigens and that the immune system itself may be perturbed by some viruses. This memorandum reviews recent developments in viral immunopathology, with special reference to animal model systems, and indicates the possible relevance of the new concepts and techniques for certain diseases of man. Certain viruses, notably the leukaemia viruses and some of those causing persistent infections, depress the host's ability to mount an antibody response to antigens, while other viruses may enhance the antibody response. Cell-mediated immunity may also be depressed. Another immunopathological manifestation of virus infection is immune-complex disease. When viruses or their antigens persist in the circulation they combine with specific antibody, and the resulting complexes lodge in various sites, especially the kidney. Further combination with complement leads to the release of tissue-damaging substances. A third condition associated with virus infection is antibody-mediated immunologic injury. Both oncogenic and non-oncogenic viruses frequently induce new antigens on the surface of the cells they invade. When antibody attaches to these antigens in the presence of complement, the cells are destroyed.
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PURPOSE: Rheumatoid arthritis is the most common systemic immune-mediated condition associated with scleritis. The purpose of this study is to determine whether or not scleritis is more severe in patients with rheumatoid arthritis than in those without associated disease ("idiopathic scleritis"), or than in patients with other systemic immune-mediated diseases. METHODS: Patient characteristics, type of scleritis, and ocular complications of 32 patients with scleritis associated with rheumatoid arthritis were compared with those of 74 patients with idiopathic scleritis and with those of 50 patients with scleritis associated with other systemic immune-mediated diseases. RESULTS: Patients with scleritis associated with rheumatoid arthritis were older (mean age, 60.78; P = 0.0011) and more often had necrotizing scleritis (34%; P = 0.0001), decrease in vision (59%; P = 0.0001), and peripheral ulcerative keratitis (31%; P = 0.0001) than patients with idiopathic scleritis; by contrast, there was no statistical association with sex, bilaterality, anterior uveitis, glaucoma, or cataract. Patients with scleritis associated with rheumatoid arthritis were older (P = 0.0261) and more often had bilateral scleritis (53%; P = 0.0221) than patients with scleritis associated with other systemic immune-mediated diseases; however, there was no statistical association with type of scleritis, sex, decrease in vision, anterior uveitis, peripheral ulcerative keratitis, glaucoma, or cataract. CONCLUSIONS: Scleritis associated with rheumatoid arthritis is more severe than idiopathic scleritis but is as severe as scleritis associated with other immune-mediated diseases.
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Systemic lupus erythematosus (SLE) was one of the first diseases to be treated by plasmapheresis, because of the abundance of serological disturbances, and the strong evidence that tissue damage is related to the deposition of immune complexes. Early results in small, uncontrolled studies were promising, but no large-scale controlled trials have yet been reported. The conditions for which well-controlled trials are now available are either diseases affecting a single organ-system, in which clinical abnormalities are readily measurable, such as Guillain-Barre syndrome, or conditions in which serological abnormalities correlate closely with clinical disturbances, such as myasthenia gravis. Definitive answers are also available in rheumatoid arthritis, where many years of clinical experience have led to the development of well-validated indices of clinical activity. Many studies of SLE suggest that serological abnormalities, though important, are often not quantitatively linked to the clinical manifestations of the disease. Attempts to develop indices of clinical activity for SLE are handicapped by the range of different organ systems which may be involved. Progress in the development of clinical trials of plasmapheresis in SLE is most likely to result from multicenter cooperative groups, which will have the capacity to study large enough numbers of patients for adequate stratification, and from the development and validation of indices of clinical activity, which will make possible the quantitation of clinical response, and the measurement of the rate of accumulation of permanent organ damage.
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Immune globulin are extracted from plasma pooled from 1000 or more donors. Each lot should contain at least 90% of intact IgG. Intravenous immune globulin are recommended unequivocally for some diseases: acute autoimmune thrombocytopenic purpura of childhood, autoimmune erythroblastopenia, haemophilia with anti-VIII antibodies, Kawasaki's syndrome, and perhaps, Guillain-Barré syndrome. Nevertheless, this therapy has been reported to be beneficial for more than 35 diseases thought to be produced by immunopathology. Large amounts of immune globulin, such as 400 to 2000 mg/kg are proposed over a period of two to five days. The safety of this treatment, which may be introduced without any special structure, is a very interesting quality of the intravenous immune globulin therapy. However, comparative efficacy against reference therapy, surveillance for long-term positive and adverse effects and cost-effectiveness should be carried out.
Transplant patients are at particular risk for developing post-transplant lymphoproliferative disease (PTLD) following administration of immunosuppressive therapy. In many cases the PTLD lesions express Epstein-Barr virus (EBV) latent and lytic genes as well as elevated levels of host cytokines. An outline of the potential contributions of EBV, host cytokines and T cells, and the immunosuppressive cyclosporine A, tacrolimus, and anti-CD3 antibody in the mechanism and pathogenesis of this disease is presented and discussed.
Retroperitoneal fibrosis is an unusual cause of obstructive uropathy in the pediatric population. The etiology is unknown although there are laboratory and clinical associations with various autoimmune diseases. Familial associations have not been reported in children. A family is reported where two siblings have idiopathic retroperitoneal fibrosis. In addition, these sisters and the father manifest clinical laboratory evidence for systemic immunologic diseases. These young girls represent the first patients to illustrate both autoimmune and familial characteristics of this disease. These cases support the concept that retroperitoneal fibrosis is a local manifestation of a systemic immune disease.
Age-associated changes in immunity, which are manifested by a reduced immune response and a greater frequency of autoimmune events, are closely linked to the pathology of ageing. Further indications that this is so are the more marked changes in immunity indices in old subjects suffering from cardiovascular, nervous and bone and joint diseases; using other indices, however, such changes appear to be less pronounced. Ageing of the immune system is accompanied by suppression of cellular and humoral elements of older individuals, as demonstrated clearly by experiments involving heterochronic parabiosis and heterochronic transplantation of cells and organs (thymus, spleen and bone marrow). Our findings may suggest that changes in the immune system with ageing are not a consequence of loss or decreases in certain cells or substances; rather, they are due to active suppression of the regulation of cell differentiation and of cooperative interaction between various types of cells. Such effects may be of a systemic or local character and reflect the expression of the organism's ontogenetic programme. In turn, primary disturbances of the immune system can cause several of the secondary ageing phenomena, dominated by various forms of pathology.
This review of scientific literature comes within the interest arisen from ten years by psychoneuroimmunology, a field connecting several disciplines and illustrating in a new way the psychosomatic relationships. A first category of works has been dedicated to the study of psychiatric disorders associated with various diseases concerning immunity (systemic diseases, endocrine diseases, cancers, infectious diseases), but also to the possible effect of distressing life events on the upset activation of immune functions, or even to the discovery of predisposing personality profiles (type C profile, depressive vulnerability). A second category of works concerns the analysis of the immune disturbances associated with certain psychiatric diseases, such as depression or schizophrenia, but also with some distressing life conditions, like bereavement. Animal experimentation and human experimentation provide various informations on the factors conditioning the immunomodulating effects of stress, sometimes in the direction of an inhibition, sometimes in the direction of an activation of immune functions. Finally, several papers shed light on the immunomodulating effects of psychotropic drugs. All these works open new horizons to the scientific knowledge and let us glimpse an extension to the use of psychologic therapeutics, as well of pharmacological ones as of non pharmacological.