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 immune response of normal human peripheral blood mononuclear cells (PBMC) after stimulation with human immunodeficiency virus-1 (HIV-1) antigens plus Leishmania donovani promastigotes in vitro was investigated. HIV-1-antigen stimulation of PBMC did not induce the intracellular accumulation of interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha), or interferon-gamma (IFN-gamma). However, cells stimulated with L. donovani antigens exhibited the production of IL-6 and TNF-alpha, but not IFN-gamma. Furthermore, co-stimulation of PBMC with HIV-1 antigen plus L. donovani resulted in the intracellular accumulation of IL-6 and TNF-alpha comparable to that of cells that were activated with L. donovani antigen alone. Heat-inactivated HIV-1 antigen did not appear to induce or suppress cytokine production by PBMC. However, the same HIV antigens did suppress L. donovani-induced proliferation as well as PPD-induced proliferation in a dose-dependent fashion. Elevated levels of serum cytokines have been demonstrated in patients with HIV infection indicating their role in the pathogenesis of HIV-associated immunosuppression. The results may partially support the idea that the abnormally increased cytokine levels in the sera of HIV-infected subjects is due to the various opportunistic pathogens that these patients contract, rather than a response to HIV antigens. As cytokines have been shown to up-regulate HIV replication, the data suggest a role for opportunistic infections in cytokine-induced transactivation of HIV-1 and disease progression.
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PMID:HIV-1 inhibits Leishmania-induced cell proliferation but not production of interleukin-6 and tumour necrosis factor alpha. 814 97

A tumour-associated antigen known as 90K has been found in high concentrations in the serum of patients infected with human immunodeficiency virus (HIV) even in the absence of neoplastic complications. In order to investigate the relationship between the production of 90K and soluble inflammatory mediators, we studied serum concentrations of the antigen, tumour necrosis factor-alpha (TNF-alpha), interleukin-I-alpha (IL-I-alpha), interferon-gamma (IFN-gamma), IFN-alpha, neopterin and beta 2-microglobulin (beta 2-m) in patients with non-neoplastic HIV infection at various stages of disease and in control persons. The antigen was detected in all those studied but its concentration was higher in HIV-infected patients compared with controls (P < 0.001), increasing progressively with advancing stages of disease. There was a negative correlation between concentrations of 90K and IL-I-alpha in patients in U.S.A. Centers for Disease Control groups II and III (P < 0.02) and also between that of 90K and both TNF-alpha (P < 0.01) and IL-I-alpha (P < 0.05) in control persons. The results indicate that 90K is not merely a tumour-associated antigen and that its production may be part of immune and inflammatory responses in the absence of neoplasia. The correlation between the concentrations of 90K and of some cytokines in asymptomatic patients and healthy persons suggests that 90K may be part of a network of immune and inflammatory reactants.
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PMID:Relationship between the tumour-associated antigen 90K and cytokines in the circulation of persons infected with human immunodeficiency virus. 816 31

Given the dissemination of acquired immunodeficiency syndrome (AIDS) in Latin America, where Chagas' disease is endemic, there is a present and increasing risk of concurrent infections with human immunodeficiency virus (HIV) and Trypanosoma cruzi. We used the model of murine acquired immunodeficiency syndrome (MAIDS) caused by a murine leukemia virus (MuLV) that induces immunologic alterations with similarities to those accompanying human HIV infection to study aspects of concomitant infections. The MuLV infection was found to reactivate T. cruzi infection in C57Bl/10 mice, as indicated by elevated parasitemia and lymphocytic infiltration in the myocardium. The T cells from these animals did not respond to T. cruzi antigens (lymphocyte proliferation, interferon-gamma, or interleukin-2 [IL-2] production) but had increased levels of IL-10. Trypanosoma cruzi-specific antibody was decreased but not absent in dually infected animals. In a second set of experiments, we infected MAIDS-resistant B6D2 mice with MuLV, followed by infection with T. cruzi. These animals had higher parasitemia than those infected with T. cruzi alone. More interestingly, only dually infected animals developed MAIDS. The present report describes the activation of T. cruzi infection by MuLV as well as the aggravation of MuLV infection by T. cruzi. These results may be relevant to coinfections with retrovirus and protozoan parasites in humans.
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PMID:Aggravation of both Trypanosoma cruzi and murine leukemia virus by concomitant infections. 825 98

Patients rendered T cell-deficient by advanced disease due to human immunodeficiency virus, an underlying neoplastic disorder, or immunosuppressive therapy are vulnerable to a select group of opportunistic infections. These infections, which often fail to respond to conventional therapy, provide the clinical setting in which the efficacy of treatment with cytokines can be tested. Particularly pertinent cytokines are those that activate macrophages and monocytes or enhance T-cell function. Experimental observations and emerging data from patients with intact T-cell function suggest that treatment with at least three cytokines, interferon-gamma, interleukin-2, and granulocyte-macrophage colony-stimulating factor (GM-CSF) may be of benefit. Each of these cytokines is already in clinical use, and each has therapeutic potential in a variety of different infectious disease. Patients with infections caused by opportunistic intracellular pathogens appear to be the most appropriate candidates for adjunctive cytokine therapy.
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PMID:Cytokines as antimicrobial therapy for the T cell-deficient patient: prospects for treatment of nonviral opportunistic infections. 827 6

The effects of inoculation of LP-BM5 murine leukemia retrovirus and chronic ethanol (5% v/v) ingestion on immunomodulation and Cryptosporidium parvum infection in C57BL/6 female mice were evaluated. The intestinal mucosae of retrovirally immunosuppressed animals were heavily colonized by Cryptosporidium parasites, and oocysts shedding in the feces persisted throughout the duration of the study. Mortality was exacerbated by murine retrovirus infection alone and exacerbated with concomitant chronic alcohol feeding (42.8 and 69.4%). Chronic ethanol ingestion decreased production of interferon-gamma and soluble interleukin-2 receptor released in supernatants of splenocytes when stimulated with concanavalin A, compared with the control group. Decreased production of interferon-gamma and interleukin-2 receptor was further exacerbated due to retrovirus infection. Tumor necrosis factor production by splenocytes stimulated with lipopolysaccharide, however, was significantly increased because of retrovirus infection. LP-BM5 retrovirus infection alone as well as with concomitant ethanol feeding altered cytokine production, which might have led to immunodeficiency. These changes may help explain the enhanced persistence of Cryptosporidiosis.
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PMID:Alcohol and murine acquired immunodeficiency syndrome suppression of resistance to Cryptosporidium parvum infection during modulation of cytokine production. 833 81

Patients with common variable immunodeficiency (CVID) are heterogeneous in the clinical manifestations of the disease and in the underlying mechanisms leading to the immunodeficiency. The impairment of B-cell function can be due to an intrinsic defect of the B cells, a deficiency in the function of the antigen-presenting cell, or a dysfunction in the course of T-cell activation. In the present report we have focused our attention on T-lymphocyte activation in three patients with CVID. Numbers of T and B cells, as well as CD4 and CD8 T cell subsets, were within the normal range. The patients' B cells secreted IgM but did not secrete IgG and IgA in response to B-cell stimuli in vitro. Addition of allogeneic T cells was followed by an increase in IgM production but had no effect on the other immunoglobulin isotypes. Examination of T-cell function revealed impaired proliferative response, interleukin-2 (IL-2) and interferon-gamma gene expression and IL-2 release after antigenic stimulation, whereas T-cell proliferation, as well as IL-2 gene expression and release in response to stimulation via anti-CD3, were comparable to those of healthy control subjects. Anti-CD3-induced IFN-gamma gene activation in T cells from two patients was comparable to that of control subjects, whereas T cells from the third patient showed reduced expression of IFN-gamma mRNA. In contrast to the decreased IL-2 and IFN-gamma mRNA levels, IL-2R transcripts examined in parallel were normal in CVID T cells on stimulation with antigen. The defect in IL-2 and IFN-gamma mRNA expression after stimulation with antigen, but not with anti-CD3, suggests an abnormality confined to T-cell activation by the T-cell receptor.
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PMID:Defective interleukin-2 and interferon-gamma gene expression in response to antigen in a subgroup of patients with common variable immunodeficiency. 834 43

Selected parameters of cellular immunity relating to cytokine gene activation and responsiveness to interleukin-2 (IL-2) were analyzed in 27 patients with active pulmonary tuberculosis and no human immunodeficiency virus type 1 infection. Cytokine mRNAs were not expressed by peripheral blood mononuclear cells (PBMC) of normal controls. In PBMC of tuberculosis patients, messages for IL-1, IL-8, and tumor necrosis factor-alpha were uniformly expressed, whereas PBMC of only 5 of 18 patients expressed IL-6. PBMC of 7 patients (all of those with systemic symptoms) expressed interferon-gamma mRNA and none expressed IL-2 mRNA. Most patients' cells demonstrated IL-4 mRNA. Limiting dilution analysis of IL-2-responsive cells in PBMC revealed that tuberculosis patients had 10-fold fewer IL-2-responsive cells than did controls.
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PMID:Cytokine gene activation and modified responsiveness to interleukin-2 in the blood of tuberculosis patients. 837 20

A double-blind, randomized, placebo-controlled trial comparing two daily doses of oral ribavirin (600 mg and 800 mg) and placebo was conducted at six medical centers. Two hundred fifteen adults were enrolled over a 5-month period and randomized to receive ribavirin 800 mg daily (74 subjects), ribavirin 600 mg (71 subjects), or placebo (70 subjects). Active treatment was administered for 24 weeks followed by a 4-week wash-out period. Fifteen patients receiving placebo, 10 receiving ribavirin 600 mg, and 18 receiving ribavirin 800 mg developed AIDS during the 28-week study period. Ribavirin at daily doses of 600 mg or 800 mg for 24 weeks did not significantly affect the rate of progression to AIDS as defined by the Centers for Disease Control, in univariate analysis, Kaplan-Meier survival analysis, or Cox proportional hazards modeling. Although in the proportional hazards analysis, the dose-response regression coefficients indicated a reduction of 43% in the hazard of progression to AIDS among patients on active treatment, it was not statistically significant (p = 0.19). Furthermore, there was no evidence that ribavirin had a significant effect upon any immunologic or virologic parameter measured, including CD4 count, CD4:CD8 ratio, lymphocyte proliferative response, skin test reactivity, interferon-gamma production, peripheral blood mononuclear cell culture for human immunodeficiency virus (HIV), or level of HIV p24 antigen in serum. The most prominent adverse effect of ribavirin was induction of a mild reversible hemolytic anemia (mean fall in hematocrit, 5%). No severe or unremitting drug reaction was documented.
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PMID:Multicenter clinical trial of oral ribavirin in symptomatic HIV-infected patients. The Ribavirin ARC Study Group. 841 72

We characterized the defects of CD4+ cells in a 17-month-old girl suffering from combined immunodeficiency with hypereosinophilia (Omenn's syndrome). Because the vast majority of peripheral blood CD4+ cells expressed the CD45R0 isoform, we purified circulating CD4+ CD45R0+ cells from the patient and healthy individuals in order to compare their production of cytokines. The patient's CD4+ CD45R0+ cells spontaneously produced high levels of interleukin-5 (IL-5) in vitro (1600 pg/ml after 24 h of culture) and this was associated with the presence of IL-5 in serum (323 pg/ml). After stimulation with phorbol 12-myristate 13-acetate (PMA) and calcium ionophore A23187, they produced higher levels of IL-4 (306 vs. 55 +/- 4 pg/ml) and IL-5 (2900 vs. 213 +/- 72 pg/ml) and lower levels of IL-2 (17 vs. 63 +/- 17 IU/ml) and interferon-gamma (IFN-gamma) (16 vs. 299 +/- 70 IU/ml) than controls CD4+ CD45R0+ cells. This T helper type 2 (Th2) pattern was confirmed by the detection using reverse polymerase chain reaction of IL-4, IL-5 and IL-10 mRNA within peripheral blood mononuclear cells. During a therapeutic trial with human IFN-gamma (40 micrograms/day) which ameliorated the clinical status of the patient, we observed a down-regulation of the in vivo expression of IL-5 and IL-10, a normalization of the eosinophil count and an improvement of the T cell response to phytohemagglutinin. This observation indicates for the first time that Th2-like cells might be involved in certain forms of congenital immunodeficiency and that IFN-gamma might down-regulate their activities in vivo.
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PMID:T helper type 2-like cells and therapeutic effects of interferon-gamma in combined immunodeficiency with hypereosinophilia (Omenn's syndrome). 841 87

We investigated serum levels of interleukin-6 (IL-6), interferon-gamma (IFN-gamma), and tumor necrosis factor alpha (TNF alpha) from patients with systemic lupus erythematosus (SLE) and its various clinical manifestations of disease and from patients with rheumatoid arthritis (RA) and other rheumatic diseases. The serum levels of IL-6 and IFN-gamma were highly elevated from patients with SLE associated with lymphadenopathy (LN) or nephrotic syndrome (NS). On the contrary, the serum levels of TNF alpha were elevated from most patients with SLE associated with thrombocytopenia (TP). However, serum levels of TNF alpha were in the normal range from patients with SLE associated with NS, LN, or central nervous system disease. Of interest, patients with SLE associated with humoral immunodeficiency disorder, hypogammaglobulinemia, had highly elevated levels of serum IL-6. The concanavalin A-stimulated mononuclear cells (MNC) of patients with SLE associated with TP secreted highly elevated levels of TNF alpha compared to other patient groups. We suggest that abnormal production of various cytokines in SLE is an intrinsic defect of MNC and the immune system that may be the key element for a variety of clinical manifestations of this disease.
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PMID:Cytokine profile in systemic lupus erythematosus, rheumatoid arthritis, and other rheumatic diseases. 844 45


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