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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Environmental interactions with the immune system may result in two types of adverse outcomes: immunodeficiency and immunopathology. Serious immunodeficiency most commonly results from ionizing radiation or as a recognized side effect of iatrogenic drug therapy, usually cancer chemotherapy. At present there is little basis for believing that biologically significant suppression of immune competence in man results from more subtle interactions with environmental agents. On the other hand, environmentally triggered immunopathology is a source of considerable morbidity and mortality. Additional research is needed in the following areas: (a) basic mechanisms of immunopathological reactions; (b) development of methods for accurately implicating or excluding immunological mechanisms in the etiology of hypersensitivity states; (c) development of methods for assessing in advance the potential immunogenicity of new industrial chemicals and occupational allergens; (d) identification of the risk factors which predispose to immunopathological outcomes when individuals are exposed to sensitizing chemicals or other "natural" allergens.
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PMID:Environmental influences on the immune system and allergic reactions. 59 54

Several distinct arthritic syndromes now have been recognized in HIV-infected persons. These comprise seronegative spondarthritis, including classic Reiter's syndrome and psoriatic arthritis associated with HLA-B27, and undifferentiated arthritis usually confined to the lower limbs, unassociated with other lesions, and unrelated to any known genetic marker. In such cases great care should be taken to exclude infection. In addition, a syndrome of short-lived but sometimes severe arthralgias also occurs. Spinal pain is a major problem in some patients but ankylosing spondylitis appears to be rare among this group. Psoriasis probably occurs more often in the HIV-infected group than in the population in general and may be especially severe in those patients with arthritis. Arthritis has been reported in the United States, Europe, and Africa among persons considered to be at high and low risk for HIV infection. Arthritis can occur at any stage of HIV infection, but the true prevalence of arthritic syndromes and the nature of their association with HIV infection remains unclear. In view of the development of Reiter's syndrome in some patients, precipitating bacterial infections have been sought as the culprits. In a minority of cases, shigella, yersinia, and campylobacter infections have been implicated, but in the majority of cases, no specific infection has been identified. In most patients depletion of circulating CD4-positive lymphocytes is present by the time that arthritis is detected, but only limited data on synovial immunopathology are available. In some patients changes of nonspecific chronic synovial inflammation are present and synovial fluid cell counts are high. In other patients evidence of inflammatory changes is minimal. Human immunodeficiency virus has been isolated from joint fluid and identified in large mononuclear, probably dendritic, cells and lymphocytes. Synovium from patients dying with AIDS but with apparently normal joints also shows significant abnormalities that could lead to joint disease in long-term survivors. The possibility of a viral etiology of arthritis in some cases is suggested by the induction of arthritis in animals by lentivirus infection; it also is possible, however, that HIV enhances the effect of mechanisms that can operate in the absence of HIV infection. Conventional treatments of rheumatic lesions, including intraarticular steroids, appear to be safe and reasonably effective. Anecdotal evidence suggests that treatment with methotrexate and azathioprine leads to exacerbation of HIV disease and should be avoided.
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PMID:Reiter's syndrome and associated arthritides. 204 87

Advances in the neurosciences and immunology provide a framework for understanding how mental health status may be a co-factor in the progression of human immunodeficiency virus (HIV) infection. The authors discuss the interrelatedness of the central nervous system and the immune system, discuss the possible relevance of such connections to HIV immunopathology, and review research that demonstrates the effect of psychiatric and psychosocial factors on immunological status and medical outcome. An application of psychoneuroimmunology to HIV infection warrants careful consideration of the many complexities involved.
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PMID:Psychoneuroimmunology and HIV infection. 213 81

Autopsy studies of AIDS (acquired immune deficiency syndrome) patients showed a high incidence of myocarditis. To attain a better understanding of the pathogenesis, the pathology and immunopathology of nine endomyocardial biopsies with active myocarditis from 18 human immunodeficiency virus (HIV)-positive patients were systematically characterized. These were compared with 17 biopsies with active myocarditis from patients without AIDS risk factors. In both groups, the myocarditis consisted of either multifocal or interstitial infiltrates of small lymphocytes and isolated myocyte necrosis. The lymphocytes consisted of T cells (CD2+, CD3+) and cells not identified by the usual markers. B cells, monocytes, CD4+ cells, and natural killer (NK) cells were only rarely observed. All of the HIV-positive patients but only 7 of 17 non-HIV patients had CD8+ lymphocytes in the infiltrates (P less than 0.01). The arteriolar endothelium demonstrated induced class I (HLA-A, B, C) and II (HLA-DR) antigens in both groups. In situ hybridization for HIV-1 failed to identify the virus in the specimens. The immunopathology is consistent with a cell-mediated injury to the myocytes in HIV-positive patients and is similar to a subgroup of myocarditis in the non-HIV group.
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PMID:HIV-associated myocarditis. Pathology and immunopathology. 226 Jun 26

The human lymphocytotropic retroviruses, despite the fact that their immunopathology varies from acute immunodeficiency to leukemia, have several features in common: they are exogenous viruses isolated from mature T cells, especially T4+ T-cells; they preferentially infect mature T4+ T cells in vitro, although other kinds of cells can be infected (no pathologic effects have been associated with infection of nonlymphoid cells); they possess a reverse transcriptase with similar size and preference for Mg++; they have a unique pX sequence in their genome which codes for a protein which is responsible for trans-activation of viral and possibly cellular genes, and in vitro infection of some T cells induces either continuous proliferation or cytotoxicity which mimic the in vivo manifestations of the virus.
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PMID:Immunopathology associated with human lymphotropic retroviruses. 242 86

Leakadine++, levamisole++, proper-myl were used in the postoperative period in 36 patients operated upon for infectious endocarditis with regard for the character of the immunopathology found. The directed immunostimulation results in resolution of immunodeficiency and normalization of the immune status of the patients.
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PMID:[Preventive use of immunostimulants in patients with infectious endocarditis]. 259 26

To further our understanding of autoimmunity, many laboratories have concentrated on the study and manipulation of murine lupus in several strains. Although direct extrapolation of data from animal to man must proceed with caution, the use of such animal systems, both in vitro and in vivo, has been an enormous help in the development of immunologic concepts. Our laboratory has been studying murine lupus by selective breeding of specific genetic immune defects onto New Zealand mice. Specifically, we have used congenital immunologic mutations resulting in asplenia (Dh/+), athymia (nu/nu) and immunodeficiency (Xid) as a means of probing the natural history of immunopathology in one such murine model of autoimmunity New Zealand (NZ) mice. These studies have provided important insights into the ontogeny of autoimmunity. NZB.Xid mice have been particularly valuable and have become a useful tool for dissecting the B cell defects of NZ mice. The Xid gene is dominant over the premature polyclonal activation of NZB mice and acts almost exclusively on B cells that are involved in autoantibody production in NZB mice. Nonetheless, the fact that autoantibody production can occur in a small percent of very old NZB.Xid mice, which have the same phenotype as other NZB.Xid mice, suggests that it can be produced by a mechanism other than a generalized polyclonal expansion and is not dependent on the circulatory or splenic frequency of the Lyb 5 subset of cells. Finally, NZB.Xid mice are unable to produce autoantibodies even after maturing in an aged NZB microenvironment, which suggests that the cell population missing in NZB.Xid mice are important for autoantibody production.
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PMID:The use of congenital immunologic mutants to probe autoimmune disease in New Zealand mice. 295 25

Studies of human immunodeficiency virus (HIV) associated lymphadenopathy by histopathology and immunopathology showed conspicuous changes of follicular B-cell areas from a marked hyperplasia to complete involution. Immunohistochemistry showed a corresponding increase in follicular dendritic reticulum cells (FDRC) followed by progressive destruction of these cells during involution, concomitant with invasion of follicles by T-cells. HIV gag antigens were predominantly associated with FDRC in hyperplastic follicles and diminished during involution. Virus replication was by in situ hybridization seen predominantly in follicles, presumably reflecting productive infection of CD4+ cells and/or FDRC. It is concluded that local effects of the virus play an important role in HIV lymphadenopathy. The marked cytopathogenic effects on FDRC indicate that HIV infection with lymphadenopathy represents not only a disease of CD4+ cells but also of follicular antigen presenting cells (FDRC).
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PMID:Lymphadenopathy in HIV (HTLV-III/LAV) infected subjects: the role of virus and follicular dendritic cells. 318 Jan 26

In studies aimed at defining monocyte and macrophage function in patients with human immunodeficiency virus (HIV) infection, we found impaired in vivo Fc receptor-specific clearance in 20 of 25 patients with acquired immunodeficiency syndrome (AIDS) and in five of 13 patients with AIDS-related illnesses. The in vivo function of macrophage C3 receptors was also found to be abnormal: AIDS patients had a relatively large release of cell back into the circulation, suggesting failure of macrophage phagocytosis. The antibody-dependent cell-mediated cytotoxicity of circulating mononuclear cells was significantly lower in AIDS patients than in healthy controls. Monocyte nonspecific phagocytosis and surface marker expression were intact. Defective monocyte and macrophage function is an integral part of the immunopathology of AIDS, leading to the failure to control opportunistic pathogens. Whether these defects are due to intrinsic infection of the mononuclear phagocytes with HIV or are secondary to other events in the network of HIV infection remains to be determined.
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PMID:Role of the mononuclear phagocyte system in the immunopathogenesis of human immunodeficiency virus infection and the acquired immunodeficiency syndrome. 270 32

Viral infections are often associated with immunodeficiency states. Although T lymphocytes have been thought to suppress the host's immune response, the precise cellular basis for this phenomenon remains unclear. Therefore, we characterized peripheral blood mononuclear cells from 9 measles virus-infected children by means of monoclonal antibodies directed against surface antigens expressed on human T lymphocytes and T-cell subsets. In addition, the measles lymphocyte blast transformation response to the T-cell mitogen phytohaemagglutinin (PHA) was evaluated as an index of specific T-cell immunocompetence. During the course of measles, there was a slight reduction in the proportion of total circulating T cells, with a relative decrease in helper-inducer and a parallel increase in suppressor-cytotoxic T lymphocytes. The PHA lymphocyte blastogenic response was found to be defective in children with measles and, interestingly, there was a significant negative correlation between the reduced PHA blast transformation value and the increased proportion of suppressor-cytotoxic cells. The biological implications of these finding with respect to the underlying immunopathology of the measles virus infection are discussed.
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PMID:Immunoregulatory T cells in measles. The relationship between reduced lymphocyte proliferative response to PHA and increased proportion of circulating suppressor-cytotoxic T cells. 623 73


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