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)

Among the various mechanisms proposed to explain the pathogenesis of cerebral lesions in human immunodeficiency virus (HIV)-induced encephalitis, a cytokine-mediated action has found most favour. Indeed, elevated expression of cytokines such as interleukin (IL)-1 and tumor necrosis factor-alpha (TNF-alpha), thought to be neurotoxic, has been found in AIDS patients. As a previous study had demonstrated the presence of HIV proviral DNA in brain tissue of a number of HIV-positive non-AIDS patients, we undertook this present investigation using morphological, immunohistochemistry (IHC) and polymerase chain reaction (PCR) methods to detect the expression of major histocompatibility complex (MHC) class II molecules, the presence of HIV-1 proviral DNA and of the cytokines TNF-alpha, IL-1 alpha, IL-4 and IL-6 in brains of the same group of individuals. The study included brains of 36 asymptomatic HIV-1 positive patients and the results were compared with those of AIDS patients either affected by HIV encephalitis (n = 8) or exempt from any neuropathological changes (n = 10) as well as of normal controls (n = 5). Results show that: HIV proviral DNA could be detected by PCR in 17 out of the 36 brains from HIV-positive pre-AIDS cases; most (15 of 17) of PCR-positive brains showed minimal to severe expression of MHC class II antigen; and cytokines could be detected predominantly within white matter even at this early stage. The data demonstrated that the state of immune activation described in AIDS is already present at the pre-AIDS stage and suggest that the presence of cytokines may already trigger the cascade of events leading to brain damage.
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PMID:Investigation on the expression of major histocompatibility complex class II and cytokines and detection of HIV-1 DNA within brains of asymptomatic and symptomatic HIV-1-positive patients. 874 Feb 30

Major histocompatibility complex (MHC) class II deficiency is an inherited autosomal recessive combined immunodeficiency, characterized by a lack of constitutive expression of the human leukocyte antigen (HLA) class II genes. The patients investigated in this study are histoidentical twin brothers with a new phenotype in MHC class II deficiency. Examination of HLA-D locus genes in their fractionated peripheral mononuclear cells (MNCs) revealed an unusual and uncoordinated mRNA pattern. Here we analyzed the distribution of pro- and anti-inflammatory cytokines expressed in these patients' adherent and nonadherent MNCs. We show that gene expression of IL-1 alpha, IL-1 beta, IL-6, granulocyte-colony-stimulating factor, and IL-10 was induced in both cell fractions, whereas increased mRNA levels of interferon-gamma and the inducible nitric oxide synthase were exclusively detected in the patients' nonadherent MNCs. As IL-10 is known to be able to downregulate transcription of MHC class II and expression of IL-10 in the patients' MNCs was increased, we investigated the regulatory function of this cytokine. Interestingly, inhibition of IL-10 protein synthesis with IL-10-specific antisense oligonucleotide DNA (IL-10-AS-ODN) induced HLA-D locus genes in these MHC class II-deficient patients. Exposure of the nonadherent cell fraction to IL-10-AS-ODN resulted in a profound induction of a previously absent DR beta 1 and DP alpha gene expression. HLA-DQ beta mRNA levels, however, were increased in both the adherent and the nonadherent MNC population. Albeit expression of HLA-D locus genes was inducible via inhibition of IL-10 translation, surface expression of HLA class II antigens on the patients' MNCs was essentially negative. The data presented support the concept of a coordinated network of pro- and anti-inflammatory cytokine regulation and this network obviously has a significant role in the cell-type-specific regulation of MHC class II expression.
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PMID:Inhibition of IL-10 protein synthesis induces major histocompatibility complex class II gene expression in class II-deficient patients. 934 39

Numerous cytokines and chemokines are involved in inflammatory and immune response. Whereas some of them inhibit virus replication in vitro directly or increase the patients' T4-lymphocyte level, others effects are not so clear. Using human immunodeficiency virus (HIV) and cell cultures we have studied the antiviral effect of complexes of salmon DNA with metals and of a new factor(s) (antiviral factor, AVF) induced in cells by the complexes. The Fe3+/DNA complex possessed the highest antiviral activity. It was found that MT-2, MT-4, CEM and Jurkat cells treated with the complexes secreted AVF which inhibited the replication of nine HIV-1 isolates, was noncytotoxic and stimulated cell proliferation. AVF did not inactivate HIV. The molecular mass analysis of AVF showed that its antiviral activity is associated with its fraction of M(r) of 3 K. Reverse transcription-polymerase chain reaction (RT-PCR) analysis of mRNA from MT-4 cells treated with the complexes showed an increase in the the expression of genes for interleukin-1 alpha (IL-1 alpha), tumour necrosis factor alpha (TNF-alpha) and TNF-beta while expression of genes for IL-1-beta, IL-2, IL-4, IL-6, IL-8. IL-10, IL-12; 35p, 40p, IL-13, GMCSF, GSF and RANTES was not detected at all. However, the anti-HIV activity of the cell culture supernatant in vitro cannot be explained by mere presence of the inflammatory substances mentioned above, because they do not possess such activity and their M(r) is higher than that of AVF. Our findings raise the possibility that AVF(s) may be involved in the mechanism of cell resistance against HIV.
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PMID:A Fe(3+)/DNA complex induces an anti-human immunodeficiency virus factor(s) in CD4+ lymphocyte cell lines. 1067 40

The purpose of this study was to quantitate levels of cytokines in parotid saliva of subjects infected with human immunodeficiency virus-1 (HIV-1) and to determine if the cytokine profiles differ in subjects with an oral opportunistic infection, i.e., candidiasis or oral hairy leukoplakia. Parotid saliva samples were obtained from HIV-infected individuals with or without candidiasis or oral hairy leukoplakia and from healthy controls and were assessed by ELISA for levels of interleukin (IL)-1, IL-2, IL-4, IL-5, IL-10, transforming growth factor-beta, tumor necrosis factor-alpha and interferon (IFN)-gamma. Saliva from HIV-infected subjects with oral candidiasis had significantly higher levels of IFN-gamma than that seen in HIV-infected individuals with no oral disease and significantly higher levels of IL-2, IL-5 and IFN-gamma than saliva of healthy controls. No significant difference was seen in cytokine levels in saliva from HIV-infected subjects with no oral infections and healthy controls. The HIV-infected subjects with oral hairy leukoplakia displayed significantly higher levels of both IL-1 alpha and IFN-gamma compared with the HIV and no oral disease group and a higher level of IFN-gamma than seen in saliva from the healthy control group. In comparing cytokine levels from both HIV and oral disease groups, significant differences were detected in levels of IL-5 and IL-10. These results indicate that the profile of salivary cytokines is altered as a result of the oral opportunistic infection candidiasis or oral hairy leukoplakia and also by concurrent HIV infection.
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PMID:Cytokine profiles in parotid saliva from HIV-1-infected individuals: changes associated with opportunistic infections in the oral cavity. 1115 69

Spontaneous secretion of interleukin 8 (IL-8) was higher in latently infected U1 cells than in acutely infected or uninfected parental U937 cells. However, the induction of IL-8 by various cytokines (IL-1 alpha, TNF-alpha, IL-6, TNF-beta, GM-CSF, IFN-gamma) was significantly reduced in U1 cells. Cytokine modulation of IL-8 production in U937 cells acutely infected with a T cell-tropic strain (IIIB) or monocytotropic strain (ADA) of human immunodeficiency virus 1 (HIV-1) (HIV-1IIIB and HIV-1ADA) was variable and showed strain-specific differences. The obtained results showed that the in vitro induction of IL-8 is impaired in promonocytic cells latently infected with HIV-1 and is differently modulated under acute conditions of infection depending on the IL-8 inducing cytokine and on the infecting virus strain.
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PMID:Cytokine-induced interleukin-8 production is depressed in chronic as opposed to acute human immunodeficiency virus 1 infection of promonocytic cells. 1115 65

Leishmaniasis has emerged as an important potential opportunistic disease among patients infected with human immunodeficiency virus type-1 (HIV-1). It has been reported that the visceral form of leishmaniasis accelerates the course of HIV-1 disease progression and shortens the life expectancy of persons in areas where both diseases are endemic. As both pathogens can infect in a productive manner the same target cell, that is, the macrophage, we examined the possible modulatory effect of the protozoan parasite Leishmania infantum on the biology of HIV-1 in primary human monocyte-derived macrophages (MDMs). We found that coinfection of MDMs with Leishmania and HIV-1 resulted in a significant enhancement of both virus transcription and release of progeny virus. The Leishmania-directed increase in HIV-1 production was associated with an increased secretion of the proinflammatory cytokines TNF-alpha and IL-1 alpha. Altogether, these findings indicate that the presence of Leishmania and HIV-1 within the same cellular microenvironment leads to an enhancement of virus gene expression. The present work also underscores the importance of studying the possible complex interactions between two human pathogens in a physiological cellular reservoir.
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PMID:Leishmania infantum enhances human immunodeficiency virus type-1 replication in primary human macrophages through a complex cytokine network. 1538 May 33


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