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 p17 matrix protein of the human immunodeficiency virus type 1 (HIV-1) plays a crucial role in AIDS pathogenesis. It orchestrates viral assembly and directs the preintegration complex to the nucleus of infected cells. Recently, the three-dimensional structure of p17 was shown to resemble that of interferon-gamma (IFN-gamma), suggesting that both proteins might share analogous functions. We demonstrate that in monocytes, p17 shares with IFN-gamma the ability to induce 1alpha-hydroxylase activity and to activate fructose 1,6-bisphosphatase gene expression in the presence of 25-hydroxyvitamin D3. However, p17 does not bind to the IFN-gamma cell membrane receptor and fails to increase expression of IFN-gamma-induced proteins, such as tryptophanyl-tRNA synthetase, Fc gammaRI, and HLA DR or B7/BB1 antigens. Altogether, our results raise the possibility that the structural resemblance between p17 and IFN-gamma causes the selective activation of a common pathway resulting in the production of 1,25-dihydroxyvitamin D3. We also found that unlike IFN-gamma, p17 increases the intracellular ATP content. Since transport of the HIV-1 preintegration complex through the nuclear membrane is an ATP-dependent process, our observation suggests that p17 plays a double role in this active transport, not only by acting as a chaperone molecule but also by recruiting the necessary energy for this process.
J Interferon Cytokine Res 1997 Aug
PMID:HIV-1 p17 and IFN-gamma both induce fructose 1,6-bisphosphatase. 928 26

The elderly are more prone to virus infections and neoplasias than are young adults. During a virus infection, interferon-alpha (IFN-alpha), proteins with antiviral, antiproliferative, and immunomodulatory properties, are transiently expressed. We here report that peripheral white blood cells from 16 subjects with a mean age of 72 years yielded less IFN when stimulated with a virus in vitro than those from 16 young adults with a mean age of 28 years. Monocytes are the main source of this IFN. However, yields of another monocyte product, interleukin-6 (IL-6), were greater in cells from the older subjects than from the young adults, so there is no general defect in monocytes from the former. Immunodeficiency in the elderly has been reported to be associated with a deficiency of zinc. When cultures of white blood cells from the elderly were supplemented with 15 microM zinc (the physiologic concentration), they produced IFN in amounts comparable to those from the younger subjects.
J Interferon Cytokine Res 1997 Aug
PMID:Zinc supplementation reconstitutes the production of interferon-alpha by leukocytes from elderly persons. 928 27

Ameboid microglia express human immunodeficiency virus 1 (HIV-1) more frequently than do ramified microglia. These two microglial subtypes might also differ in the frequency with which they express transforming growth factor-beta1 (TGF-beta1), a cytokine that regulates HIV-1 expression in monocytes. Results described here show that ameboid and ramified microglia express TGF-beta1. In brain tissues from HIV-1-infected individuals as compared with seronegative controls, ameboid rather than ramified microglia more frequently expressed TGF-beta1. Ameboid microglia, isolated and cultured from postmortem adult human brain more frequently expressed TGF-beta1 in presence of interleukin-1(IL-1), a cytokine that is elevated in brains of HIV-1-infected individuals when compared with seronegative controls. The stimulation of TGF-beta1 by IL-1 was dose and time dependent, occurring with ameboid microglia isolated from either frontal cortex or globus pallidus but not midbrain pons. Ameboid microglia are similar to the RCA-1-positive cells that form clusters, called microglial nodules, in the brain of HIV-1-infected individuals. Pathologic conditions, such as disseminated microglial nodules, are associated with HIV-1 encephalitis, direct infection of the brain, and moderate to severe neurologic impairment. TGF-beta1 expression in ameboid microglia may play a role in HIV-1 neuropathogenesis.
J Interferon Cytokine Res 1997 Nov
PMID:Transforming growth factor-beta1 in adult human microglia and its stimulated production by interleukin-1. 940 3

The current study examined the proliferative capacity and cytokine secretion pattern of peripheral blood mononuclear cells (PBMC) from human immunodeficiency virus type 1 (HIV-1)-infected patients in response to the major surface glycoprotein (MSG) of Pneumocystis carinii. PBMC from AIDS patients with <200 CD4 cells/mL had significantly less proliferative responses to MSG than did healthy controls. Cytokine analysis indicated that interferon-gamma secreted in response to MSG was also significantly less. There was no significant difference in interleukin-4 levels following incubation with MSG between any of the groups; however, all the HIV-infected persons had slightly elevated levels. When the CDC class C3 patients who had a previous episode of P. carinii pneumonia were compared with those who had not had a previous episode, there was a significant increase in the proliferative response to MSG and in interleukin-4 secretion. CDC class C3 patients who had a previous episode of P. carinii pneumonia showed a predominately Th2 response to MSG.
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PMID:Proliferative and cytokine responses of human T lymphocytes isolated from human immunodeficiency virus-infected patients to the major surface glycoprotein of Pneumocystis carinii. 941 98

Chronic hemodialysis (HD) patients have defects in cell-mediated immunity. To investigate the mechanisms underlying this immunodeficiency, we studied the production of cytokines in peripheral blood mononuclear cells (PBMC) from HD patients. PBMC from 22 HD patients and 20 healthy controls were cultured for 48 h in the presence or absence of phytohemagglutinin (PHA), lipopolysaccharide (LPS), or tuberculin purified protein derivative (PPD). Cytokine levels were measured by enzyme-linked immunosorbent assays. Only 64% of HD patients had a positive tuberculin skin test compared to 90% of normal Japanese controls. HD patients showed a diminished proliferative response to PHA. Compared to healthy controls, stimulated PBMC from HD patients produced similar amounts of T cell-derived cytokines (interleukin-2 (IL-2) and interferon-gamma (IFN-gamma)), but greater amounts of monocyte-derived inflammatory cytokines (IL-1 beta, tumor necrosis factor-alpha (TNF-alpha), and IL-8) and a regulatory cytokine (IL-10). IL-10 production was positively correlated with IL-1 beta and TNF-alpha in healthy controls, whereas no correlation was observed in HD patients. Abnormal cytokine production by monocytes may contribute to the immunodeficiency seen in HD patients.
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PMID:Increased production of interleukin-10 and inflammatory cytokines in blood monocytes of hemodialysis patients. 943 12

This article reviews developments over nearly 15 years in the application of interferon-alpha (IFN-alpha) to the treatment of Kaposi's sarcoma (KS) in patients with acquired immunodeficiency syndrome (AIDS). The initial success of IFN treatment for selected patients with AIDS-associated KS occurred before identification of the human immunodeficiency virus (HIV) and in the absence of any coherent view of KS pathogenesis. A more comprehensive understanding of the biology of both AIDS and KS, together with increased knowledge of the biologic effects of IFN and therapeutic advances in the treatment of HIV infection, have made IFN therapy for KS both more rational and more successful. There is every reason to believe that the current results with IFN for KS can be improved on by capitalizing on recent improvements in HIV therapy and the availability of specific inhibitors of angiogenic cytokines. I sincerely thank the Milstein family and my colleagues in the International Society for Interferon and Cytokine Research (ISICR) for recognizing this work, which is the product of many collaborations between clinical and basic scientists in my own institution and elsewhere.
J Interferon Cytokine Res 1998 Apr
PMID:Interferon-alpha: evolving therapy for AIDS-associated Kaposi's sarcoma. 956 21

Human immunodeficiency virus-associated nephropathy (HIVAN) is the third leading cause of end-stage renal failure in Blacks between the ages of 20 and 64. Because the incidence of HIV infection has continued to increase in Blacks as survival has improved, the pool of patients alive and at risk for developing HIVAN has vastly expanded. This suggests that HIVAN will continue to increase in importance to the end-stage renal disease program. The racial predilection for the disease in Blacks implies that genetic or environmental cofactors are involved. Evidence in human and animal models has shown that proliferation of renal epithelial cells is the predominant feature of the disease and that apoptosis occurs. The prospect that renal infection is necessary to stimulate cells to proliferate remains a possibility but is not yet proven. Cytokine dysregulation may also be involved in disease progression, but evidence is lacking that altered cytokine production is the proximate cause of HIVAN. Many issues remain to be resolved including the potential for renal infection in vivo, the mechanisms responsible for proliferation and apoptosis, and factors that provide racial susceptibility to HIVAN. Advances in our understanding of pathogenesis will be required to control the growth of HIV-related renal diseases in the ESRD population.
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PMID:Pathogenesis of human immunodeficiency virus (HIV)-associated nephropathy. 969 55

Similar to human immunodeficiency virus, feline immunodeficiency virus (FIV) induces immunodeficiency and enhanced susceptibility to secondary pathogens. To explore cytokine alterations in lentivirus immunodeficiency, constitutive mRNA expression was measured in lymph nodes of healthy and FIV-infected cats before and after challenge with Toxoplasma gondii. Cytokine mRNA expression was similar in control and FIV-infected cats during the first 10 weeks after infection. At 16 weeks, interferon (IFN)-gamma, tumor necrosis factor-alpha, and interleukin (IL)-10 mRNA were increased in FIV-infected cats. Challenge with T. gondii induced an increase in IL-2, IFN-gamma, and IL-12 in the lymph nodes of control cats, whereas IFN-gamma and IL-10 but not IL-2 or IL-12 increased in the lymph nodes of FIV-T. gondii coinfected cats. These results indicate that FIV immunodeficiency may derive from a failure to generate an IL-12-dependent type 1 response and that an elevated level of IL-10 mRNA expression is a predictor of lentivirus immunodeficiency.
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PMID:Elevated interleukin-10-to-interleukin-12 ratio in feline immunodeficiency virus-infected cats predicts loss of type 1 immunity to Toxoplasma gondii. 969 33

CD4+ lymphocytes constitute one of the major cell targets for human immunodeficiency virus type 1 (HIV-1) infection. The eventual loss of CD4+ lymphocytes contributes substantially to the pathogenesis of HIV-1 and development of acquired immunodeficiency syndrome (AIDS). CD4+ lymphocytes consist of the subgroups Th1, Th2, and Th0, which differ in their cytokine profile. Th1 cells produce cytokines that favor cell-mediated immune responses, whereas Th2 cells produce cytokines that favor humoral immunity. Th0 cells are precursors to the Th1 and Th2 subsets. A shift from a Th1 to a Th2 response has been reported for HIV-1-infected patients (Kannagi et al. 1990. J. Virol. 64, 3399-3406; Walker et al. 1986. Science 234, 1563-1566; Walker et al. 1991. J. Virol. 65, 5921-5927). For this reason, the potential role of cytokines in the development of AIDS has received a great deal of attention. Interleukin (IL)-12 is a disulfide-linked, 70-kDa heterodimeric cytokine produced by antigen-presenting cells. IL-12 has a central role in the development of the Th1-type immune responses. Therefore, we investigated the ability of T-tropic HIV-1 IIIB to replicate in Th1, Th2, and Th0 T cell clones and studied the effects of IL-12 on HIV-1 replication in these cells types. These studies demonstrate several points. (1) Th1, Th2, and Th0 T cell clones support HIV-1 IIIB replication nearly equally well, and it is, therefore, unlikely that differences in ability to support HIV-1 replication can explain changes in Th1, Th2, or Th0 subtype 1 following HIV-1 infection. (2) Using this model, we show that IL-12 can inhibit HIV-1 replication, consistent with a role for IL-12 in HIV-1 replication in T cells. (3) HIV-1 can form a persistent infection in T cell clones, providing a reservoir model for study of viral sanctuary and persistence in a system closely approximating the in vivo situation.
J Interferon Cytokine Res 1998 Jul
PMID:Infection of T cell subsets by HIV-1 and the effects of interleukin-12. 971 68

We previously reported that intramuscular (i.m.) immunization of DNA vaccine encoding human immunodeficiency virus type 1 (HIV-1)IIIB env and rev genes alone or in combination with appropriate adjuvant induces substantial and enhanced immune response against HIV-1. In the present study, we examined whether a polymer, low-viscosity carboxymethylcellulose sodium salt (CMCS-L), has an adjuvant effect on immune response induced by DNA vaccination. BALB/c mice were immunized with HIV-DNA vaccine formulated with CMCS-L via the intranasal (i.n.) and i.m. routes. The combination with the polymer elicited higher levels of antigen-specific serum IgG and fecal IgA antibodies than DNA vaccine alone. For cell-mediated immunity, HIV-specific delayed-type hypersensitivity response and cytotoxic T lymphocyte activity were measured by the footpad-swelling test and the 51Cr-release assay, respectively. Both were enhanced by the combination with CMCS-L via i.n. and i.m. inoculation. Cytokine analysis in culture media of bulk splenocytes harvested from immunized animals showed higher levels of IL-4 production in i.n. -immunized mice compared with i.m.-immunized mice. Nevertheless, the increased IFN-gamma production resulting from the combination with CMCS-L was observed only in i.n.-immunized mice. These data indicate that i.n. immunization of HIV-DNA vaccine formulated with CMCS-L enhances HIV-specific mucosal antibody (Ab) and systemic Ab and cell-mediated immune response.
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PMID:Intranasal administration of HIV-DNA vaccine formulated with a polymer, carboxymethylcellulose, augments mucosal antibody production and cell-mediated immune response. 971 99


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