Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004364 (autoimmune disease)
 24,845 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Essential fatty acid (EFA) deficiency is known to alter the immune response in several experimental systems. To further evaluate the effects of EFAs on immunity Lewis rats were fed diets either adequate or deficient in EFAs for 70-80 days. EFA-adequate rats responded to an i.v. injection of 5 X 10(8) sheep erythrocytes with a sharp, short-lived rise in splenic levels of PGE and PGF within 2 minutes after injection. EFA deficiency resulted in a diminution of this PG response. PG production in liver homogenates was also depressed in EFA-deficient liver. An i.v. injection of sheep erythrocytes resulted in a humoral response against this antigen, measured as hemolytic plaque-forming cells in the spleen. EFA deficiency, as well as pretreatment of EFA-adequate rats with indomethacin, an inhibitor of PG synthesis, resulted in a stimulation of the plaque-forming cell response over that observed in control, EFA-adequate rats. The alterations in immune response resulting from changes in PG synthetic capacity may be important in the etiology of certain immunodeficiency syndromes such as the lupus-erythematosus-like autoimmune disease in NZB/W mice.
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PMID:Essential fatty acid deficiency, prostaglandin synthesis and humoral immunity in Lewis rats. 634 64

Using the protein A haemolytic plaque assay (PrA-HPA) and standardized, optimal conditions, pokeweed mitogen (PWM) stimulated peripheral blood lymphocytes (PBL) from normal donors produced 5,500-48,000 (mean 16,955) IgG plaque-forming cells (PFC) per 10(6) lymphocytes, 3,375-38,000 (mean 14,179) IgA-PFC/10(6) and 5,500-69,750 (mean 18,684) IgM-PFC/10(6). Addition of 4 micrograms/ml concanavalin A (Con A) at the start of PWM stimulation of PBL from normal donors gave 59-98% (mean 84%) suppression of IgG-PFC, 46-99% (mean 79%) suppression of IgA-PFC and 31-100% (mean 82%) suppression of IgM-PFC. When PFC/10(6) values in PWM-stimulated co-cultures of unfractionated PBL from pairs of unrelated normal donors were compared with PFC/10(6) obtained in the individual PWM-stimulated cultures, observed/expected ratios were between 0.81 and 1.24 (mean 0.99) for IgG-PFC, 0.85 and 1.23 (mean 0.98) for IgA-PFC and 0.86 and 1.25 (mean 1.03) for IgM-PFC. Cord blood lymphocytes (CBL) produced few PWM-stimulated PFC and co-culture of CBL with normal PBL gave markedly reduced observed/expected ratios, indicating hyperactivity of T-suppressor cells in cord blood. PBL from a patient with partial DiGeorge syndrome also responded poorly in the PWM-driven PrA-HPA, but co-culture of this patient's PBL with normal PBL and PWM gave rise to higher than expected values, indicating reduced T-helper cell function. These simple methods could be employed in clinical evaluation of the cellular defect in humoral immunodeficiency and autoimmune disease states.
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PMID:Clinical evaluation of B cell and T-regulator cell function using a protein A haemolytic plaque assay. 646 53

The relationship between colony formation (cloning) of B cells and their activation in murine autoimmunity was investigated in MRL-lpr/lpr and MRL.xid mice. Cells from MRL-lpr/lpr mice showed similar requirements for in vitro growth as normal CBA/J and BALB/c cells, with maximal colony formation in the presence of the supporting factors lipopolysaccharide and sheep red blood cells. The frequency of colony-forming cells from MRL-lpr/lpr spleens or hapten-specific B-cell preparations was slightly greater than the two normal control strains, with this difference significant only for a comparison of BALB/c and MRL-lpr/lpr spleens. In contrast, MRL-lpr/lpr mice bearing the xid gene for B-cell immunodeficiency (MRL.xid) had markedly reduced B-cell colony formation. These mice nevertheless expressed anti-DNA antibodies, although at levels reduced from that of MRL-lpr/lpr controls. These results indicate that enhanced in vitro colony formation need not accompany B-cell hyperactivity in murine autoimmune disease and that autoantibody production can occur in mice with impairment in this growth property.
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PMID:Cloning of B cells from autoimmune MRL-lpr/lpr and MRL.xid mice. 660 79

Impairment of any of the major components of the immune system (T-cells, B-cells phagocytes, complement) may result in clinical immunodeficiency. Immune defects can arise from intrinsic or heritable defects of lymphoid elements, failure of normal cellular differentiation, viral infection or other acquired causes. Clinical impairment of immunity is expressed as a marked susceptibility to opportunistic and pathogenic organisms which are difficult to control and by an increased risk of malignancy, allergy and autoimmune disease. Certain immunodeficiency disorders are associated with aberrant immune regulation. The major types of immune deficiency are characterized by unique patterns of infections depending on the level at which the defect occurs and the pathogenic mechanisms of the parasite. The basic defects of representative primary and secondary immunodeficiencies are discussed in relation to observed immunologic consequences.
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PMID:Diseases associated with immunosuppression. 703 90

We describe a child with primary defect of polymorph bacterial killing associated with systemic lungs erythematosus. We suggest that her autoimmune disease results from chronic bacterial antigen stimulation and propose a hypothetical model linking immunodeficiency with autoimmunity.
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PMID:A polymorph bactericidal defect and a lupus-like syndrome. 725 60

Recent progress in the definition of molecules involved in immune regulation has led to the discovery of a number of type I membrane glycoproteins with a distinctive, cysteine-rich, repetitive domain structure within their extracellular regions. Because the prototype members of this family are receptors for cytokines (tumor necrosis factor [TNF] and nerve growth factor [NGF]), it was expected that the ligands for the other receptors would possess cytokine-like activities. This prediction has been fulfilled by the cloning of cDNA encoding a series of type II membrane glycoproteins, with homology to TNF, that bind to, and signal through, their cognate receptors. While the biological role of some of these ligand-receptor pairs remains obscure, at least two members of the family, CD40 and Fas, have proven their importance. The human X-linked immunodeficiency, hyper IgM syndrome, is the result of mutations in the CD40 ligand gene, and the Fas and Fas ligand genes are mutated in two mouse strains, lpr and gld, that develop autoimmune disease. These findings, together with other evidence, point to key roles of CD40/CD40 ligand interactions in immune activation, particularly in T-dependent B cell responses, and of Fas/Fas ligand in apoptosis and peripheral tolerance. These molecules, as well as the other ligands of the family, share the property of costimulation of T cell proliferation and are all expressed by activated T cells. More detailed analysis of the expression patterns of ligands and receptors on lymphocyte subpopulations will be necessary to define their different roles in immune activation and suppression.
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PMID:A family of ligands for the TNF receptor superfamily. 752 88

Immunological abnormalities have been described in patients with Hodgkin's disease, both associated with the malignancy itself and occurring secondary to therapy. These abnormalities often manifest as an immunodeficiency state, but can also present as immune dysregulation and autoimmune disease. We report two young patients with Hodgkin's disease who, following successful therapy, developed urticarial vasculitis (UV), a form of cutaneous autoimmune vasculitis. Both patients also had systemic symptoms including fever, an elevated erythrocyte sedimentation rate and serum copper, and abnormal in vitro studies of lymphocyte enumeration and proliferation. Distinguishing UV from recurrent Hodgkin's disease was especially difficult in one patient, and was possible only by lymph node biopsy. One patient has responded well to immunosuppressive therapy, while the other, who has more profound immune dysfunction, has developed a chronic autoimmune disorder. UV may thus occur in patients after therapy for Hodgkin's disease; we hypothesize that immune dysregulation, either associated with the malignancy or resulting from therapy, is important in the pathogenesis of this autoimmune process.
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PMID:Urticarial vasculitis: an autoimmune disorder following therapy for Hodgkin's disease. 762 31

Aberrant production of antibodies has been reported in some patients infected with human immunodeficiency virus. However, manifestations of autoimmune disease are rare. A case of a human immunodeficiency virus seropositive patient with a high titer of antinuclear antibodies and clinical manifestations of psoriasiform subacute cutaneous lupus erythematosus is described.
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PMID:Lupus-like eruption and human immunodeficiency virus infection. 763 45

Studies of cell population dynamics and microenvironmental organization of B lymphopoiesis in the bone marrow of normal mice and in various genetically modified states have shown that cell loss, involving processes of apoptosis and macrophage-mediated cell deletion, is a prominent feature of the primary genesis of B lymphocytes. Balanced against the influence of proliferative stimulants, the programmed death of precursor B cells provides a quantitative control, determining the magnitude of the final output of functional B lymphocytes to the peripheral immune system. The cell loss mechanisms can be readily set in motion by external or systemic influences, making the B-cell output particularly vulnerable to suppression by ionizing irradiation, stress or other systemic mediators. In addition, however, cell loss exerts an important quality control in the formation of the primary B-cell repertoire. The combination of apoptosis and macrophage-mediated deletion, acting at successive stages of B-cell differentiation, efficiently eliminates many precursors having non-productive Ig gene rearrangements, cell cycle dysregulations, and certain autoreactive Ig specificities. Outstanding areas of further work abound. Important questions concern the nature of mechanisms which underlie the processes of B-cell apoptosis and macrophage deletion in bone marrow, the microenvironmental signals involved in B-cell life or death decisions and genetic factors which may override these B-cell culling mechanisms. The answers will be relevant to problems of autoimmune disease, humoral immunodeficiency and B-cell neoplasia.
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PMID:Apoptosis and macrophage-mediated cell deletion in the regulation of B lymphopoiesis in mouse bone marrow. 769 95

Although the exact mechanisms by which superantigens may contribute to the pathogenesis of diseases are unknown, it seems increasingly likely that they have a role in the induction and pathogenesis of disease. The studies described here demonstrate that in several different diseases either bacterial or viral superantigens can be isolated from patients. There is also a preferential expansion of particular V beta T-cell subsets, which is a common feature of superantigen stimulation. From the work that has been done to date it can be hypothesized that superantigens may act in several ways. They may stimulate and activate T cells that are autoreactive and lead to the induction or exacerbation of autoimmune disease, as in RA. Alternatively, they may lead to the depletion of T-cell subsets based on V beta expression, thereby resulting in the severe reduction in lymphocytes in certain immunodeficiency diseases such as AIDS. But perhaps the most likely contribution of superantigens to disease pathogenesis is seen indirectly by their effect on the immune system-particularly the stimulation of large numbers of T lymphocytes expressing the same V beta domain. Thus it is likely that the direct effect of various T-cell-derived inflammatory mediators (i.e., interleukins and other cytokines) released by these activated T lymphocytes is the primary cause of disease pathology via response to superantigen stimulation. In addition to the diseases discussed here, there are a number of other diseases in which a potential role for superantigens is being studied. These include autoimmune diseases seen after group A streptococcal infections in which the streptococcal M protein has been postulated to act as a superantigen such as scarlet fever, rheumatic heart disease, and poststreptococcal glomerulonephritis. Other diseases being studied include psoriasis, lupus-like disease, and lymphoproliferative diseases (reviewed in Kotzin et al.). In the coming years the exact role of superantigens and the specific mechanisms by which they contribute to disease should be more clearly defined. Our understanding of these molecules could also lead to new therapies for the treatment of these diseases.
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PMID:Superantigens and their role in infectious disease. 771 12


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