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

Human immunodeficiency virus (HIV) strains can be separated into two types: HIV and HIV-related West African viruses. Site-directed serology using synthetic peptides offers possibilities for the determination of type-specific antibodies. A 22-amino-acid peptide with the sequence Ala-Ile-Glu-Lys-Tyr-Leu-Glu-Asp-Gln-Ala-Gln-Leu-Asn-Ala-Trp-Cys-Ala-Phe-Arg-Gln - Val-Cys representing a conserved region of the transmembranous protein of simian T-cell lymphotropic virus-type III (STLV-III; related to West African HIV) was used as antigen in an enzyme-linked immunosorbent assay (ELISA). In parallel, tests were performed with a pair of previously described peptides, including the homologous region of the glycoprotein (gp) 41 of the HIV strain HTLV-IIIB. In tests with three groups of 20 sera it was shown that the different peptide ELISAs allowed a categorical distinction of antibodies to the two types of HIV. Tests using peptide antigens may provide excellent opportunities for large-scale testing for type-specific antibodies against HIV. The tests are simple, sensitive and specific and are readily standardized.
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PMID:Discrimination between antibodies to HIV and to related retroviruses using site-directed serology. 304 Dec 32

We evaluated the cellular immunity of 408 clinically stratified subjects at risk for acquired immune deficiency syndrome (AIDS), to define the role of interferon-alpha production deficits in the pathogenesis of opportunistic infections (OI). We followed 115 prospectively for up to 45 mo. Onset of OI was associated with, and predicted by, deficiency both of interferon-alpha generation in vitro, and of circulating Leu-3a+ cells. Interferon-alpha production is an index of the function of certain non-T, non-B, large granular lymphocytes (LGL) that are independent of T cell help. Leu-3a+ cell counts are a marker of T cell function. OI did not usually develop until both of these mutually independent immune functions were simultaneously critically depressed, leading to a synergistic interaction. These data suggest that the AIDS virus affects a subset of LGL, and that cytokine production by these cells is an important component of the host defense against intracellular pathogens that becomes crucial in the presence of severe T cell immunodeficiency.
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PMID:Opportunistic infections in acquired immune deficiency syndrome result from synergistic defects of both the natural and adaptive components of cellular immunity. 308 39

Irradiated CBA/J mice transplanted with H-2 compatible, minor histocompatibility disparate B10.BR bone marrow develop graft-versus-host disease (GVHD) if mature T lymphocytes are added to the marrow inoculum. In the setting of mild GVHD (receiving 10(4) or 10(5) T cells), by phenotypic analysis, lymphoid reconstitution occurs normally within 4 to 6 wk but there is a profound deficiency in the ability of splenic lymphocytes to respond to polyclonal activators such as LPS and Con A. This unresponsiveness is attributable to active suppression mediated by cells that express Thy-1 and can be removed with leucine methyl ester treatment. Thus, splenocytes from mice with GVHD suppress responses of normal T and B lymphocytes. Moreover, depletion of these suppressor cells restores normal function to splenocytes from mice with GVHD, and B cells isolated from these mice respond normally to T-dependent and -independent stimulation. Finally, IFN-gamma plays an important role in this suppression, because a neutralizing anti-IFN-gamma mAb significantly removes suppression of normal cells and restores functional responses of lymphocytes from mice with GVHD. These results provide insights into the mechanisms of immunodeficiency associated with GVHD, and suggest novel strategies for possible therapies for this disorder.
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PMID:Immunodeficiency in graft-versus-host disease. I. Mechanism of immune suppression. 312 5

Peripheral blood mononuclear (PBM) cells from five of 21 patients with common variable immunodeficiency (CVI) stimulated in vitro by antigen produced antibodies normally. In 11 of the 16 non-responders, removal of adherent suppressor cells by Sephadex G-10 or removal of monocytes or OKT8 positive suppressor lymphocytes by other means of separation made antibody responses demonstrable. Cells adherent to the G-10 column had suppressor function in the autologous antigen driven system; the suppressor activity appeared to be due to adherent T cells in some patients and to adherent monocytes in others. The suppressor cell functions in these patients did not correlate significantly with the number of cells positive for monoclonal antibodies OKT8 or Leu-2. Factors suppressing antibody production in this system were found in normal serum but usually not in serum of the patients with CVI studied. Substances in normal serum which enhance antibody production in this system when added late in culture were present in serum of patients with CVI. Any abnormality of interleukin-1 production by monocytes of these patients did not seem relevant to the immunodeficiency.
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PMID:B-cell function in common variable immunodeficiency: suppression of in vitro anti-sheep erythrocytes antibody production by T cells and monocytes. 315 90

Lymphocyte subpopulations and macrophages in 16 spleens from patients with Hodgkin's disease were analysed immunohistochemically using monoclonal antibodies of the Leu and the Ki M series. In non-involved splenic tissue there is an increase of T-lymphocytes with an increased T-helper/T-suppressor cell ratio, while Ki M-1, -2, -3 and -5-positive, i.e. phenotypically different macrophages, are reduced. These results indicate that involvement of the spleen in Hodgkin's disease is accompanied by changes with respect not only to lymphocyte subpopulations but also to cells of the mononuclear phagocyte system. The immunodeficiency associated with Hodgkin's disease is probably not solely due to lymphocyte dysfunction, since the disease may lead, at least in the spleen, to alterations in macrophages and accessory cells and this may contribute to the impairment of cell-mediated immunity.
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PMID:The spleen in Hodgkin's disease. An immunohistochemical study of lymphocyte subpopulations and macrophages. 316 83

Alterations in polymorphonuclear leucocyte (PMN) function are frequently associated with intraoral disease. The purpose of this study was to evaluate if alterations exist in three early stimulatory events of PMN function in individuals with intraoral manifestations of human immunodeficiency virus (HIV) infection. Peripheral PMNs were isolated from nine HIV-seropositive male homosexuals with HIV-associated periodontitis and intraoral candidiasis and healthy HIV-seronegative age-matched heterosexuals (controls). Phagocytosis was assessed using fluorescent microspheres, oxidative burst was assessed via hydrolysis of 2',7'-dichlorofluorescein (FCDH) to 2',7'-dichlorofluorescein (FCDA) with PMA stimulation, and F-actin formation was assessed with NBD-phallacidin stain after stimulation with f-Met-Leu-Phe. Compared to controls, seven of nine HIV-seropositive patients demonstrated a significant increase in the percentage of phagocytic cells while seven of nine HIV-seropositive patients demonstrated a 5-59% increase in number of beads per cell. In the oxidative burst assay, seven of seven HIV-seropositive patients demonstrated a significant increase over controls in FCDA stain with PMA stimulation. In the F-actin assay, four of five HIV-seropositive patients demonstrated a significant increase over controls in NBD-phallacidin staining after f-Met-Leu-Phe stimulation.
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PMID:Elevated phagocytosis, oxidative burst, and F-actin formation in PMNs from individuals with intraoral manifestations of HIV infection. 321 15

Employing a novel panel of monoclonal antibodies, we characterized in detail the quantitative immunopathologic alterations of lymph nodes in a 69-year-old heterosexual man who died of acquired immunodeficiency 1.5 years after transfusion of blood products. Absolute decreases were evident in total T cell, helper T cell, cytotoxic T cell, and Leu 8+ cell counts. Suppressor T cells and histiocytes were absolutely increased. There were relative increases in B cells and Leu 7+ cells. B-cell follicles were sparse and exhibited small, burned-out germinal centers composed predominantly of R4/23+ dendritic reticulum cells. These findings closely paralleled those described previously for homosexual men with acquired immunodeficiency syndrome (AIDS). They suggest that AIDS occurring among diverse clinical groups, such as homosexual men and blood donor--recipient pairs, involves similar immunopathologic alterations within lymph node microenvironments.
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PMID:Fatal post-transfusion acquired immunodeficiency in a heterosexual man: quantitative lymph node immunopathology. 325 45

The antigenic phenotype of human villous stromal macrophages (M phi s) from first and third trimester placentas was analyzed using a large number of monoclonal antibodies (MAbs) to monocyte (Mo)/M phi-associated cell membrane determinants. The purpose of this study was to investigate M phi phenotypic heterogeneity to create a database for the correlation of M phi phenotype with specific immunologic functions. The results showed that villous stromal mononuclear cells express many cell surface antigens found on Mo and M phi s and that they are morphologically diverse, ranging in appearance from classic Hofbauer cells to spindle-shaped cells with long cytoplasmic processes. Villous stromal M phi s were the numerically dominant cell type in this structure and exhibited some major phenotypic differences from M phi s in other tissues. Comparison of first- and third-trimester placentas revealed variation in antigen expression with increasing gestational age, in particular of class II major histocompatibility complex (MHC) determinants: HLA-DR and HLA-DP antigen density was low on first-trimester villous M phi s and much higher on third-trimester M phi s while HLA-DQ was undetectable in the first trimester but present on cells in third trimester placentas. The CD1 (T6) antigen, found on Langerhans (LH) cells and cortical thymocytes, was detected on villous M phi s by two thirds of the MAbs directed against different epitopes on this determinant. Furthermore, comparison with similar studies of lymphoid tissues showed that villous M phi s and dendritic cells share the expression of a number of other cell surface antigens. Finally, it was shown that M phi s in first- and third-trimester villi exhibit strong reactivity with MAbs (Leu 3a,b) to the CD4 antigen that serves as the receptor for the human immunodeficiency virus (HIV), suggesting that these cells may be a portal of entry or reservoir for this virus in the fetuses of pregnant, HIV+ women.
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PMID:The phenotype of human placental macrophages and its variation with gestational age. 326 59

Cytolytic activity of human mononuclear peripheral blood leukocytes from healthy donors, cultured in interleukin-2 conditioned medium, was abrogated by in vitro infection with the lymphadenopathy associated virus (LAV) isolate of the human immunodeficiency virus (HIV). Although viral antigens are not expressed in cultured cells until 14 days postinfection, cytolytic activity was lost as early as 3 days after infection. Loss of cytolytic function was not a result of the release of suppressive factors from either infected cells or uninfected CEM cells since supernatants from neither infected cultures nor CEM cell cultures had any inhibitory effects on the function of uninfected cells. Cultured lymphocytes expressing Leu 11b were also shown to express HIV antigens via immunofluorescence after 14 days in culture. These results suggest that natural killer (NK) cells, as defined by expression of Leu 11b, were infected by HIV in vitro and the loss of lytic function was likely a direct consequence of that infection.
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PMID:Natural killer cell infection and inactivation in vitro by the human immunodeficiency virus. 328 79

Human-human B cell hybridomas constructed from B lymphocytes of common variable immunodeficiency (CVI) patients and the nonsecreting cell line WIL2/729 HF consistently secrete low levels of Ig and appear to retain a defect characteristic of the CVI patient's B cells. We assessed the differentiative capacity of retinoic acid (RA) on these hybridomas, as well as on hybridomas constructed from normal B cells and from patients with selective IgA deficiency. RA at concentrations varying between 10(-5) and 10(-9) M augmented IgM secretion 4-20-fold from four of four CVI hybridomas tested, but did not affect Ig secretion from normal or IgA-deficiency hybridomas. In support of this elevated Ig secretion, RA enhanced the de novo synthesis of biosynthetically labeled light (kappa) and heavy (mu) Ig (up to 4- and 15-fold, respectively) in the CVI hybridoma line JK32.1. The increase in IgM synthesis/secretion could not be accounted for by RA-induced alteration in the cell cycle. In inducing this increase in IgM production, RA was found to affect two aspects of Ig gene expression: (a) the steady-state levels of heavy and light chain mRNAs were enhanced, and (b) the processing of mu heavy chain transcripts to the secreted mRNA form became favored over the membrane mRNA form. We also show that expression of Leu-17 (CD38), a surface marker that is re-expressed in the late pre-plasma stage of B cell development, was increased by RA from less than 20% to greater than 90% of the total cell population, with a concomitant 4-10-fold augmentation in the mean fluorescence intensity. Changes in both Leu-17 expression and de novo Ig synthesis were prominent by 24 h, but could be observed as early as 8 h after induction. Taken together, our study demonstrates that RA affects a marked alteration in the differentiated state of the CVI hybridoma clones. This finding suggests that retinoids can enhance the functional capabilities of B cells with defects in maturation and support further studies to evaluate their clinical potential in CVI.
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PMID:Retinoic acid induces the differentiation of B cell hybridomas from patients with common variable immunodeficiency. 329 36


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