Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cell lineage and cell function antigens were studied immunohistochemically in human immunodeficiency virus-associated oral Kaposi's sarcoma to provide insight into tumor pathogenesis. All tumors were composed predominantly of spindle cells that expressed endothelium-associated antigens, CD34 and CD36 (factor VIII-related antigen was expressed by considerably fewer numbers of tumor cells). Infrequently, spindle tumor cells also expressed actin. Factor XIIIa positive spindle and dendritic stromal cells comprised up to 9% of the tumor cell population. Other spindle and dendritic cells expressing macrophage-associated antigen, CD68, accounted for up to 15% of the tumor cells. Mast cells occurred frequently within and around tumors. Leukocyte function antigen (CD18) was expressed by approximately 13% of tumor cells, and its ligand, intercellular adhesion molecule (ICAM), was expressed by some tumor-associated capillaries (which also expressed endothelial leukocyte adhesion molecule, ELAM) and occasional stromal cells. Staining for proliferating cell nuclear antigen was noted in both interstitial and vascular lining cells. All tumors were non-reactive for human Papillomavirus antigen and HIV p24 antigen. Oral KS is a heterogeneous cellular proliferation composed predominantly of endothelial or endothelium-related spindle cells. Other spindle/dendritic (XIIIa-positive and CD68-positive) cells and mast cells are also present and may contribute to tumor development. ICAM and ELAM expression within tumors may assist infiltration of macrophages and other inflammatory cells into these lesions.
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PMID:Human immunodeficiency virus-associated oral Kaposi's sarcoma. A heterogeneous cell population dominated by spindle-shaped endothelial cells. 810 Apr

Cytopathic mechanisms in human immunodeficiency virus type 1 (HIV-1) infection involve syncytia formation, and it appears likely that increased expression of intracellular adhesion molecule 1 (ICAM-1) is involved in these cell adhesion phenomena. In this study, we determined serum concentrations of soluble ICAM-1 (sICAM-1) in 27 patients with HIV-1 infection and a control group. In addition, we compared sICAM-1 values to CD4+ T-cell counts, serum beta 2-microglobulin (beta 2M) and serum neopterin levels. HIV-1-infected patients had significantly higher sICAM-1, beta 2M and neopterin levels than controls. The subgroup of patients with Walter-Reed stages 3-6 had only slightly higher sICAM-1 concentrations in serum than Walter-Reed stages 1-2. The sICAM-1 concentrations in HIV-1-seropositive patients correlated with beta 2M levels but neither with neopterin nor with CD4+ T-cell counts. Increased sICAM-1 may result from immune activation, which enhances the expression of ICAM-1 in patients with HIV-1 infection.
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PMID:Increased levels of serum intercellular adhesion molecule 1 in HIV infection are related to immune activation. 810 76

The human immunodeficiency virus type 1 (HIV-1) external envelope glycoprotein gp120 tightly binds CD4 as its principal cellular receptor, explaining the tropism of HIV-1 for CD4+ cells. Nevertheless, reports documenting HIV infection or HIV binding in cells lacking CD4 surface expression have raised the possibility that cellular receptors in addition to CD4 may interact with HIV envelope. Moreover, the lymphocyte adhesion molecule LFA-1 appears to play an important role in augmenting HIV-1 viral spread and cytopathicity in vitro, although the mechanism of this function is still not completely defined. In the course of characterizing a human anti-HIV gp41 monoclonal antibody, we transfected a CD4-negative, LFA-1-negative B-cell line to express an anti-gp41 immunoglobulin receptor (surface immunoglobulin [sIg]/gp41). Despite acquiring the ability to bind HIV envelope, such transfected B cells could not be infected by HIV-1. These cells were not intrinsically defective for supporting HIV-1 infection, because when directed to produce surface CD4 by using retroviral constructs, they acquired the ability to replicate HIV-1. Interestingly, transfected cells expressing both surface CD4 and sIg/gp41 receptors replicated HIV much better than cells expressing only CD4. The enhancement resided specifically in sIg/gp41, because isotype-specific, anti-IgG1 antibodies directed against sIg/gp41 blocked the enhancement. These data directly establish the ability of a cell surface anti-gp41 receptor to enhance HIV-1 replication.
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PMID:Enhanced in vitro human immunodeficiency virus type 1 replication in B cells expressing surface antibody to the TM Env protein. 810 54

Infection of the rhesus monkey with simian immunodeficiency virus of macaques (SIVmax) was employed to explore the early immune events associated with the initial containment of an acute AIDS virus infection. In nine rhesus monkeys infected intravenously with uncloned SIVmac strain 251, high-level p27 plasma antigenemia was usually detected transiently from approximately day 7 through day 21 following virus inoculation. SIVmac replication in lymph nodes measured by in situ RNA hybridization closely paralleled the time course and magnitude of viremia. The containment of SIVmac spread by 3 to 4 weeks following infection suggests an efficient, early immune control of this virus infection. Anti-SIVmac antibodies were first detected in the blood at approximately day 14. At the time antigenemia was decreased or cleared, SIVmac neutralizing antibodies were present. A rise in circulating and lymph node CD8+ T cells also occurred coincident with the clearance of antigenemia and persisted thereafter. These CD8+ lymphocytes in lymph nodes had increased expression of both major histocompatibility complex class II and the adhesion molecule LFA-1; they also demonstrated decreased expression of the naive T-cell-associated CD45RA molecule. SIVmac-specific cytotoxic T-lymphocyte precursors were detected in both blood and lymph node by 7 days post-virus inoculation. These studies indicate that both virus-specific humoral and cellular immune mechanisms in blood and lymph node are associated with the clearance of viremia that occurs within the first month of infection of rhesus monkeys with SIVmac.
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PMID:Immunopathogenic events in acute infection of rhesus monkeys with simian immunodeficiency virus of macaques. 813 22

Impaired polymorphonuclear neutrophil (PMN) function may contribute to the onset of certain bacterial and fungal infections and to tissue damage in human immunodeficiency virus (HIV)-infected patients. Published data on PMN function in HIV infection are controversial, possibly because most studies have involved PMNs isolated from the normal blood environment by various procedures that may modify PMN responses. We therefore used flow cytometry to study the expression of adhesion molecules at the PMN surface, actin polymerization, and the oxidative burst of whole-blood PMNs in 42 HIV-infected patients at different stages of the disease. These PMNs were activated in vivo, as shown by increased expression of the adhesion molecule CD11b/CD18, reduced L-selectin antigen expression, increased actin polymerization, and increased H2O2 production. The alterations were present in asymptomatic patients with CD4+ cell counts above 500/microliters and did not increase with progression of the disease. This PMN activation could contribute to the oxidative stress described in HIV infection. Stimulation by bacterial N-formyl peptides showed dysregulation of L-selectin shedding and decreased H2O2 production after cx vivo priming with tumor necrosis factor-alpha or interleukin-8. These latter impairments, which correlated with the decrease in CD4+ lymphocyte numbers, could contribute to the increased susceptibility of HIV-infected patients to bacterial infections.
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PMID:Impairment of polymorphonuclear neutrophil function in HIV-infected patients. 869 65

Despite the relatively early reconstitution of blood B-lymphocyte counts observed in patients treated with bone marrow transplantation (BMT), these patients undergo a prolonged phase of humoral immunodeficiency. Adhesion molecules perform relevant functions in many cell types. The present study examines the expression of several adhesion molecules on human B lymphocytes newly formed after BMT. Blood B cells from 38 patients were studied by flow cytometry and three-color analysis. Blood CD5- B lymphocytes obtained at an early stage after BMT (2 to 4 months) showed a markedly low expression of the adhesion molecules CD54, CD44, CD11a, and CD62L. However, these cells exhibited a normal expression of other molecules including CD29, CD19, CD20, and DR. This deficiency was progressively corrected, reaching normal levels in the late post-BMT period (12 to 15 months). In contrast, CD54, CD44, CD11a, and CD62L expression on the patients' CD5+ B lymphocytes was found to be consistently normal. Deficient adhesion molecule expression on CD5- B cells in the early post-BMT period was similarly observed in patients treated with either an allo-BMT (n = 24) or an auto-BMT (n = 14). Because the post-BMT period mimics normal ontogeny, adhesion molecule expression was also investigated in cord-blood B lymphocytes. Cord-blood CD5- B lymphocytes, in contrast to CD5+, also expressed CD54, CD44, CD11a, and CD62L at levels much lower than those found in normal adults. Present data suggest that progressive expression of CD54, CD44, CD11a, and CD62L seems to be a part of the maturational program of CD5- B lymphocytes during both post-BMT and normal development periods. This observation may help to explain the humoral immunodeficiency observed in both conditions.
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PMID:Deficient expression of adhesion molecules by human CD5- B lymphocytes both after bone marrow transplantation and during normal ontogeny. 878 29

The ability of Hymenolepis nana oncosphere extract to induce eosinophil chemotactic response was examined in vitro and in vivo. The extract showed a chemotactic activity specific for eosinophils but not for neutrophils. Partially purified eosinophil chemotactic factors (ECFs) from the oncosphere extract showed apparent molecular mass from 5.5 to 9.6kDa and 30 to 40kDa. These were resistant to heating and proteinase K digestion but sensitive to periodate oxidation. Peritoneal injection of the crude extract or partially purified ECFs to mice resulted in a preferential eosinophil infiltration. The chemotactic activity for eosinophils was not separable from the adhesion molecule expression or oxygen radical-inducing activity by means of chromatography or chemical treatments. Furthermore, histological examination demonstrated a marked tissue eosinophilia around H. nana larvae in the intestinal lamina propria of both humoral and cell-mediated immunodeficiency mice. The present findings suggest that H. nana oncosphere-derived molecules facilitate in vivo the intestinal eosinophilia during the infection.
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PMID:Enhancement of intestinal eosinophilia during Hymenolepis nana infection in mice. 896 Jan 97

Immune-mediated mechanisms appear to play a primary role in the pathogenesis of polymyositis (PM) and dermatomyositis (DM). The serum of patients with active DM has high levels of circulating complement fragments C3b, C4b, and C5b-9 membranolytic attack complex (MAC) and demonstrates a very high C3 uptake in an vitro assay system. The MAC and the immune complex-specific C3bNEO fragment are deposited on the endomysial capillaries early in the disease and lead sequentially to loss of capillaries, muscle ischemia, muscle fiber necrosis, and perifascicular atrophy. In contrast, in PM the muscle fiber injury is initiated by sensitized CD8+ cytotoxic T cells that recognize heretofore unknown and probably endogenous muscle antigens in the context of major histocompatibility complex (MHC) class I expression. A restricted (oligoclonal) pattern of T-cell receptor with prominence of Va1, Vb6, and Vb15 genes is noted within the endomysial infiltrates suggesting that the T-cell response is antigen driven. In both PM and DM, intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 are upregulated in the endomysial endothelial cells and function as ligands for the leukocyte integrins leukocyte function-associated antigen (LFA)-1 and very late activating antigen (VLA)-4, allowing activated lymphocytes to adhere to the endothelial cells and migrate to the muscle fibers. Among viruses, only the retroviruses human immunodeficiency virus (HIV) and human T-cell lymphotropic virus (HTLV)-1 have been convincingly shown to trigger PM, which is mediated by nonviral-specific, cytotoxic CD8+ cells. The treatment of inflammatory myopathies remains empirical. Many patients respond to steroids to some degree and for some period of time. Azathioprine, methotrexate, cyclosporine, cyclophosphamide, and plasmapheresis can be of mild to moderate benefit. High-dose intravenous immunoglobulin (IVIg) is a promising therapeutic modality for some patients resistant to therapies. In a controlled study, IVIg was effective in DM not only in improving the clinical symptoms but also in reversing the underlying immunopathology. The role of IVIg in PM and IBM is under study in control trials.
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PMID:Immunopathogenesis of inflammatory myopathies. 896 19

In addition to gp41 and gp120, an array of cell adhesion molecules is present on the envelope of human immunodeficiency virus type 1 (HIV-1). To examine the role of the host cell in the acquisition of these molecules by virions, both laboratory-adapted and primary isolates were sequentially passaged into different host cells. Viruses obtained from the various host cells were examined for the presence of 10 different cell-derived molecules by a virus binding enzyme-linked immunosorbent assay. Virus progeny raised in peripheral blood mononuclear cells expressed most of the adhesion molecules tested, with the level of LFA-1 being the highest. When viruses were passaged into CEM-SS or SupT1 cells, the expression of most of the adhesion molecules on the virus envelope was lost. In contrast, when viruses were passaged into MT2 cells, the virus progeny bore high levels of LFA-3, ICAM-1, and major histocompatibility complex classes I and II. These studies demonstrate for the first time the host cell dependence of the adhesion molecule profile present on the envelope of primary isolates of HIV-1. The presence of several adhesion molecules that have not previously been identified as components of the envelope of either laboratory or primary isolates is also described. In addition, we show that the adhesion molecule profile of the virions is acquired, or lost, within one passage and is maintained with subsequent passages in the same cell type.
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PMID:Host cell-dependent alterations in envelope components of human immunodeficiency virus type 1 virions. 909 15

Incorporation of the intercellular adhesion molecule ICAM-1 into human immunodeficiency virus type 1 (HIV-1) particles increased virus infectivity on peripheral blood mononuclear cells (PBMCs) by two- to sevenfold. The degree of ICAM-1-mediated enhancement was greater for viruses bearing envelope glycoproteins derived from primary HIV-1 isolates than for those bearing envelope glycoproteins from laboratory-adapted strains. Treatment of target PBMCs with an antibody against LFA-1, a principal ICAM-1 receptor, was able to nullify the ICAM-1-mediated enhancement. The incorporation of ICAM-1 rendered HIV-1 virions less susceptible to neutralization by a monoclonal antibody directed against the viral envelope glycoproteins. Surprisingly, an antibody against ICAM-1 completely neutralized infection by ICAM-1-containing viruses, reducing the efficiency of virus entry by almost 100-fold. Thus, HIV-1 neutralization by an ICAM-1-directed antibody involves more than an inhibition of the contribution of ICAM-1 to virus entry.
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PMID:Contribution of virion ICAM-1 to human immunodeficiency virus infectivity and sensitivity to neutralization. 915 84


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