Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

The degree of clinical severity in human immunodeficiency virus infected patients, ranging from asymptomatic seropositive subjects to acquired immune deficiency syndrome, as well as in individuals at risk was assessed in relation to: (1) T-cell subset balance and expression of markers of T-cell activation; (2) natural killer activity; and (3) interferon gamma production. A decrease in the CD4/CD8 (helper/suppressor) ratio and an increase in the percentage of CD8+ (suppressor/cytotoxic) cells coexpressing markers of activation (HLA-DR or CD25) were closely correlated with the clinical severity of the human immunodeficiency virus infection. Natural killer activity was significantly impaired in patients with acquired immune deficiency syndrome and acquired immune deficiency syndrome-related complex but normal in asymptomatic seropositive individuals and subjects at risk. Interferon gamma production, either in response to mitogens or the antigens from infectious agents commonly affecting human immunodeficiency virus-positive individuals, was decreased in patients with acquired immune deficiency syndrome or acquired immune deficiency syndrome-related complex, with lesser involvement in human immunodeficiency virus-seropositive subjects or individuals at risk. Four of the six persons in the last group seroconverted during the ten months subsequent to evaluation of their immune status. Since production of interferon gamma was diminished in these patients while other assays of immunity were normal, measurement of this lymphokine may be a useful determinant of infection with the human immunodeficiency virus.
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PMID:Diminished interferon gamma production may be the earliest indicator of infection with the human immunodeficiency virus. 297 56

Six patients with the acquired immune deficiency syndrome (AIDS) had exacerbations or recurrences of previously quiescent atopic disease when they developed immunodeficiency. Four developed a different atopic illness from that suffered previously. Atopic symptoms developed within three months after the patients developed AIDS or during prodromal illness. Two of the patients were treated with recombinant interferon gamma: both showed a striking improvement in symptoms and cellular immunity. These results indicate that cellular immunity, through interferon gamma, may have a role in regulating atopic disease.
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PMID:Atopic manifestations in the acquired immune deficiency syndrome: response to recombinant interferon gamma. 310 72

Tests for lymphoproliferation and interferon induction in normal blood donors and patients with rheumatoid arthritis (RA) were performed in a whole-blood assay. Patients with high inflammatory RA showed significantly reduced lymphoproliferation and interferon gamma production after stimulation with phytohemagglutinin (PHA) and concanavalin A (Con A) when compared with patients with low inflammatory activity, or with normal control individuals. Similarly, patients with high and low inflammatory RA exhibited a significantly reduced interferon alpha production after stimulation with Newcastle Disease Virus (NDV) when compared with normal blood donors. Our findings may point to an important immunodeficiency of the circulating lymphocytes of RA patients and may explain some of the in vitro immunoregulatory abnormalities reported in this disease.
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PMID:Reduced production of interferon alpha and interferon gamma in leukocyte cultures from patients with active rheumatoid arthritis. 311 75

To fully characterize the relationship between the clinical manifestations of human immunodeficiency virus infection and T4+ cell defects, we determined T4+ cell number and interferon gamma (IFN-gamma) production in 238 patients. For asymptomatic homosexuals, patients with acquired immunodeficiency syndrome (AIDS)-related complex (ARC), and patients with fully established AIDS, clinical status correlated linearly with both T4+ cell number and T4+ cell-derived (antigen-stimulated) IFN-gamma secretion. For asymptomatic homosexuals, abnormalities in T4+ cell number and IFN-gamma generation were similar irrespective of human immunodeficiency virus seropositivity. For patients with ARC, those with lymphadenopathy (LA) alone or LA plus zoster or thrombocytopenia displayed T4+ cell defects similar to those observed in asymptomatic homosexuals. Patients with ARC with LA plus constitutional symptoms and/or oral thrush, however, had fewer T4+ cells, were strikingly more deficient in IFN-gamma production, and closely resembled those with AIDS. Among patients with AIDS, certain individuals with Kaposi's sarcoma (KS) alone were sufficiently less cytopenic and less immunodeficient than patients with opportunistic infections (Ols) to suggest that the immune impairment that predisposes to KS may differ. At the time patients with KS developed Ols, however, T4+ cell number and IFN-gamma-generating capacity had declined to the remarkably low levels observed in virtually all patients with Ols alone.
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PMID:T4+ cell production of interferon gamma and the clinical spectrum of patients at risk for and with acquired immunodeficiency syndrome. 256 1

Dehydration-rehydration liposome vesicles (DRVs) containing various cytokines were evaluated for their ability to induce delayed-type hypersensitivity (DTH) and humoral immunity to the recombinant envelope protein rgp120 of the MN strain of human immunodeficiency virus type 1 (HIV-1). The DRVs trapped approximately 25% of the radiolabeled cytokines and approximately 17% of the radiolabeled rgp120 that were added. The level of trapping was greater than the aqueous volume of the DRVs, indicating association of the proteins with the lipid bilayer. Flow cytometric analysis using antibody to rgp120 or the V3 loop of rgp120 showed the diameter of the DRVs to be 2-7.5 microns. Transmission electron microscopy confirmed the heterogeneity in size of the DRVs and revealed morphological heterogeneity. Transmission electron microscopy with immunogold labeling also revealed the presence of rgp120 on the surface of the DRVs. In vitro bioassays demonstrated slow leakage of biologically active cytokines from DRVs soaked in tissue culture medium containing serum. Mice injected subcutaneously three times at 14-day intervals with DRVs containing 15 micrograms of rgp120 plus interleukin 6 (IL-6) or interferon gamma (IFN-gamma) produced significantly greater DTH responses than mice injected with DRVs containing rgp120 alone. Soluble rgp120 plus soluble IFN-gamma produced DTH in some experiments, but of lower magnitude than the comparable DRVs. Interleukin 6, but not IFN-gamma, increased the antibody titer to rgp120 when included in the DRVs. The mice did not develop antibodies to IFN-gamma or IL-6. Induction of DTH by vaccines may increase protection from viral pathogens such as HIV. Cytokine-containing liposomes may be an effective adjuvant for the induction of a DTH response to envelope-antigen subunit vaccines.
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PMID:Cytokine-containing liposomes as adjuvants for HIV subunit vaccines. 749 39

Human immunodeficiency virus (HIV) infection leads to a progressive loss of CD4+ T helper (Th) type 1 cell-mediated immunity that is associated with defective in vitro CD4+ T cell proliferation and abnormal T cell death by apoptosis in response to T cell receptor (TCR) stimulation. Quantification of interleukin (IL)-2, interferon gamma, IL-4, IL-5, and IL-10 secretion by immunoassays, and of interferon gamma, IL-4 and IL-10 messenger RNA expression by competitive reverse transcriptase polymerase chain reaction after in vitro stimulation of the TCR revealed a similar Th1 cytokine profile in T cells from HIV-infected persons and from controls. These data indicated that the loss of CD4+ Th1 cell function in HIV-infected persons is not related to a Th1 to Th2 cytokine switch as previously proposed, but to a process of activation-induced death of CD4+ Th1 cells. Despite the absence of elevated levels of Th2 cytokines, apoptosis of CD4+ T cells, but not of CD8+ T cells, was prevented in vitro by antibodies to IL-10 or IL-4, two Th2 cytokines that downregulate Th1 cell responses, or by the addition of recombinant IL-12, a cytokine that upregulates Th1 functions. TCR-induced apoptosis of T cell hybridomas and preactivated T cells has been shown to involve the CD95 (Fas/Apo-1) molecule. CD4+ and CD8+ T cells from HIV-infected persons expressed high levels of the CD95 molecule, and, in contrast to T cells from controls, were highly sensitive to antibody-mediated CD95 ligation, which induced apoptosis in a percentage of T cells similar to that induced by TCR stimulation. As TCR-induced apoptosis, CD95-mediated apoptosis of CD4+ T cells, but not of CD8+ T cells, was prevented by the addition of recombinant IL-12. Together, these findings suggest that apoptosis of CD4+ T cells from HIV-infected persons involves an abnormal sensitivity to CD95 ligation, and to TCR stimulation in the presence of normal levels of Th2 cytokines. The preventive effect of IL-12 on both mechanisms has potential implications for the design of immunotherapy strategies aimed at the upregulation of CD4+ Th1 cell functions in AIDS.
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PMID:T helper type 1/T helper type 2 cytokines and T cell death: preventive effect of interleukin 12 on activation-induced and CD95 (FAS/APO-1)-mediated apoptosis of CD4+ T cells from human immunodeficiency virus-infected persons. 750 20

We investigated the CD8+CD57+ alveolar cell functions and their immunoregulatory role in lungs from HIV-seropositive patients with the clinical presentation of lymphocytic alveolitis at different stages of human immunodeficiency virus (HIV) disease. We previously reported, at Stage IV of HIV infection, an expansion of CD8+CD57+ alveolar lymphocytes mirroring the decline of local anti-HIV cytotoxic T-lymphocyte (CTL) responses, and demonstrated that sorted CD8+CD57+ alveolar lymphocytes inhibited the effector phase of these HIV-specific CTL. In the present study, we show that the expansion of CD8+CD57+ alveolar T cells can also be detected at stages II and III of HIV disease, although at a lower degree than observed at Stage IV of HIV infection. When sorted, these CD8+CD57+ alveolar lymphocytes block effector killer cells such as allospecific CTL, natural killer (NK), and lymphokine-activated killer (LAK) cells. The mechanism of action of these inhibitory T-lymphocytes has been further studied and we demonstrated that: (1) cell-to-cell contact between inhibitor and killer is not required, (2) nonstimulated alveolar CD8+CD57+lymphocytes but not CD57- lymphocytes spontaneously release a solube inhibitor of cytolytic functions (ICF). This inhibitory activity of alveolar CD8+CD57+ cells is mediated by a glycosylated protein which is distinct from tumor necrosis factor-alpha (TNF alpha), TNF beta, transforming growth factor-beta 1 (TGF beta 1), TGF beta 2, interferon alpha (IFN alpha), interferon gamma (IFN gamma), and prostaglandins. The release of such an inhibitor of killer cell functions by CD8+CD57+ lymphocytes in the lungs, which are an important interface between the sterile body and the antigen-laden environment, may play a role in the local control of cell immunity.
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PMID:Alveolar CD8+CD57+ lymphocytes in human immunodeficiency virus infection produce an inhibitor of cytotoxic functions. 751 68

The effects of bovine immunodeficiency-like virus (BIV) on monocyte function were examined in experimentally infected cattle and in monocytes infected in vitro. Infection with the R29 isolate of BIV appeared to have relatively little effect on monocyte function in cattle during the first 2 years postinfection (PI). For the first 4 to 8 months post infection, monocyte phagocytosis of Staphylococcus aureus tended to be lower (P = 0.06) in BIV infected calves than in control animals. After 8 months PI, however, phagocytosis became equal between the two groups. Random and chemotactic migration and antibody-dependent cell-mediated cytotoxicity (ADCC) did not appear to be affected by BIV infection. Monocytes from BIV infected cattle were able to respond to in vitro treatment with interferon gamma similarly to monocytes from control cattle. Although experimental infection with BIV R29 resulted in minimal effects on monocyte function, this result could have been due either to a low virus burden in vivo or because BIV is intrinsically unable to affect monocyte function. To distinguish between these possibilities, monocytes from control, uninfected cattle were treated with BIV virus in vitro. Treatment of normal monocytes with cell-free virus significantly (P < 0.05) increased phagocytosis and random and chemotactic migration and decreased ADCC, in a dose-dependent manner. It appears, therefore, that the normal function of peripheral blood monocytes in the BIV R29 infected animals may be due to a low virus burden rather than to the inability of BIV to affect monocyte function. The in vitro infection results also raise the possibility that the function of monocyte derived cells at local sites of BIV replication may be altered.
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PMID:Monocyte function in cattle experimentally infected with bovine immunodeficiency-like virus. 760 36

Increased levels of serum IgE and eosinophilia have been described in human immunodeficiency virus (HIV) infection, almost exclusively in patients with CD4+ cell count < 200 cells/microliters. IgE production is regulated by CD4+ T helper type 2 (Th-2) lymphocytes, producing interleukin 4 (IL-4) and expressing a ligand for the B cell-specific CD40 molecule (CD40 ligand [L]). A shift to a Th-2-like pattern of cytokine secretion has been postulated to be associated with progression toward acquired immunodeficiency syndrome (AIDS). We studied three AIDS patients with very high levels of IgE and almost complete depletion of CD4+ lymphocytes, suggesting that IgE synthesis could not be driven by CD4+ cells. IgE in vitro synthesis by cells from such patients was, however, inhibited by anti-IL-4. We show that both CD8+ T cell lines and the majority of CD8+ T cells clones derived from these patients produce IL-4, IL-5, and IL-6 in half of the cases together with interferon gamma (IFN-gamma). 44% of CD8+ T cell clones expressed a CD40L, and the supernatants of the clones were capable of inducing IgE synthesis by normal B cells costimulated with anti-CD40. CD8+ T cells in these patients therefore functionally mimic Th-2 type cells and may account for hyper-IgE and eosinophilia in the absence of CD4+ cells. The presence of such CD8+ cells may also provide a source of IL-4 directing the development of predominant Th-2 responses in HIV infection.
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PMID:CD8+ T lymphocytes provide helper activity for IgE synthesis in human immunodeficiency virus-infected patients with hyper-IgE. 780 25

Cytokine production of unstimulated and mitogen-stimulated peripheral blood mononuclear cells of 31 children vertically infected with human immunodeficiency virus type 1 (HIV) and with different patterns of disease progression was evaluated to establish possible correlations between the immunologic and the clinical findings. Production of interferon gamma and interleukin-2 (type 1 cytokines), and of interleukin-4 and interleukin-10 (type 2 cytokines), was analyzed in seven symptom-free patients (Centers for Disease Control and Prevention class P-1B), 10 patients with mild symptoms (class P-2A), and 14 patients with severe symptoms (class P-2B-F). Cytokine production was compared with that of 10 age- and sex-matched control subjects who were seronegative for HIV. The HIV-infected patients produced significantly fewer type 1 cytokines and significantly more type 2 cytokines than the uninfected control subjects. No differences in the production of interferon gamma and interleukin-2 were detected among the different clinical categories of HIV-infected patients. In contrast, interleukin-4 production was augmented in the patients with class P-2A (p < 0.05) and class P-2B-F HIV infection (p < 0.03), in comparison with the children with class P-1B infection. The increase in interleukin-4 production was paralleled by an increase in the number of children with hyperimmunoglobulinemia E in each of the clinical groups (0% in class P-1B; 40% in class P-2A; and 71% in class P-2 B-F infection). Similarly, interleukin-10 production was increased both in patients with class P-2A and in those with class P-2B-F infection, in comparison with the children with class P-1B disease (p < 0.006 and < 0.04, respectively). These data indicate (1) that vertically acquired HIV infection results in decreased production of type 1 cytokines and in increased production of type 2 cytokines, and (2) that an increased production of type 2 cytokines correlates with hyperimmunoglobulinemia E and is present in, and may be characteristic of, the symptomatic phases of childhood HIV infection.
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PMID:Immunologic characterization of children vertically infected with human immunodeficiency virus, with slow or rapid disease progression. 786 94


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