Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peyer's patch (PP) T cells through the production of appropriate cytokines foster the development of immunity to the intestinal protozoan parasites such as Giardia. T cell destruction by the human immunodeficiency virus precedes the development of acquired immune deficiency syndrome. Thus, HIV may increase susceptibility to intestinal parasite infections. Therefore, we measured the resistance and T cell cytokine responses to Giardia in C57B1/6 mice infected with the retrovirus LP-BM5 which produces a murine AIDS (MAIDS). Mice with MAIDS and controls were intragastrically challenged with 1 x 10(5) G. muris cysts. Fecal counts were measured weekly following challenge. Also, PP T cell production of interleukin (IL)2, IL3, IL4, and Interferon-gamma in response to G. muris trophozoite antigens displayed on antigen presenting cells were measured at these times. Prior to day 14 of the infection, the number of Giardia cysts in the retrovirus group paralleled that in controls. However, by day 21 after Giardia infection, mice with MAIDS failed to clear the Giardia cysts from the intestine while the control mice were completely free of cysts. IL2 and IL4 production in response to Giardia trophozoites by unfractionated PP lymphocytes were severely depressed in the retrovirus infected group, while IFN-gamma production was increased. Depressed cytokine production was most likely due to depressed PP T cell numbers. When fractionated enriched T cells were adjusted to a uniform concentration in in vitro immunization cultures, the production of IL2 and IL4/IL5 were similar between retrovirus infected compared with control mice. Recoverable PP T cells were lower in mice with MAIDS.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Suppression of resistance to Giardia muris and cytokine production in a murine model of acquired immune deficiency syndrome. 129 11

Interferon-gamma (IFN-gamma) has been shown to inhibit human immunodeficiency virus (HIV) replication in macrophages. However, the site of its effect on the HIV infectious cycle is unknown. We show here that IFN-gamma inhibits the transactivation of HIV long terminal repeat (LTR) during viral infection and that it antagonizes tat effect in HT4LacZ-1 cells. HT4LacZ-1 is an indicator CD4+ HeLa cell line for HIV infectivity, because it harbors a HIV LTR-LacZ gene susceptible to transactivation by tat. It was used in combination with a computer-assisted image analyzer to quantify: (i) the number of transactivated foci following HIV infection, (ii) their individual level of transactivation, and (iii) the fusion potency of infected cells. IFN-gamma induced a 75% decrease of the number of transactivated foci following infection of HT4LacZ-1 cells by HIV. The remaining 25% foci still susceptible to transactivation were transactivated at a lower level than in control cultures, and the fusion potency of infected cells was strongly decreased. IFN-gamma acted after HIV entry into the cell and independently of reverse transcription. IFN-gamma antagonized tat-induced LTR transactivation: it inhibited transactivation of HT4LacZ-1 cells when tat was provided either from a SV40-based expression vector of tat or by polyethylene glycol-induced cell fusion with HeLa-tat-III cells. These results suggest that IFN-gamma affects the expression or the activity of cellular factors interacting with tat and that the high level of IFN-gamma production associated with HIV infection plays a role in the establishment of HIV latency.
 ...
PMID:Antagonistic effect of interferon-gamma on tat-induced transactivation of HIV long terminal repeat. 140 Mar 76

We describe an unusual example of cellular immunodeficiency associated with interleukin-2 deficiency in an otherwise healthy 15-year-old boy who had isolated cryptococcal osteomyelitis of the scapula at 10 years of age. His previous medical history was remarkable only for prolonged, severe varicella infection at 6 years of age. He had persistent moderate lymphopenia, anergy, and absent lymphocyte blastogenic responses to mitogens, antigens, or monoclonal T cell antibodies. Subnormal blastogenic responses were seen after exposure to high concentrations of phorbol esters. Immunoglobulin levels and specific antibodies were normal. The patient has been in good health since treatment of his osteomyelitis. However, his lymphocyte blastogenic responses to mitogens have remained absent during 4 years of observation; investigation of the cause revealed a specific interleukin-2 deficiency resulting from defective generation of interleukin-2 messenger ribonucleic acid. Secretion of interleukin-1 by monocytes was normal, suggesting that the abnormal blastogenic response and interleukin-2 production were due to a problem intrinsic to T lymphocytes. The generation of messenger ribonucleic acid for interleukin-4 was not affected. Interferon-gamma was produced at subnormal levels. The addition of recombinant interleukin-2 restored lymphocyte blastogenic responses and increased the expression of interleukin-2 receptors. The clinical findings and immunologic abnormalities present in this patient differ from other primary and secondary immunodeficiencies associated with interleukin-2 deficiency. Thus our observations in this patient extend the spectrum of immunodeficiencies associated with abnormalities in the production of this important cytokine.
 ...
PMID:Cryptococcal osteomyelitis and cellular immunodeficiency associated with interleukin-2 deficiency. 144 48

Interferon-gamma-induced protein 10 is a 10-kd protein produced by human keratinocytes following an exposure to interferon gamma. Keratinocytes within psoriatic plaques and within delayed-type hypersensitivity reactions have been shown to stain strongly with an affinity-purified rabbit antibody prepared against interferon-gamma-induced protein 10, suggesting a possible role for interferon gamma in the production of the lesions. A psoriasiform eruption has been seen in patients with acquired immunodeficiency syndrome (AIDS). Its severity appears to correlate with the degree of immunodeficiency in the early stages of AIDS. We stained 10 lesions of psoriasiform dermatitis of AIDS with the anti-interferon-gamma-induced protein 10 antibody using immunoperoxidase techniques. As controls, we studied 10 lesions of non-AIDS psoriasis, six lesions of seborrheic dermatitis with psoriasiform hyperplasia, one lesion of lichen simplex chronicus, and four biopsy specimens of normal skin from patients with AIDS. In addition, normal skin specimens taken from patients with AIDS and human immunodeficiency virus-negative patients at time of autopsy were examined. An identical, strong and diffuse staining pattern was seen in all cases of psoriasiform dermatitis of AIDS, non-AIDS psoriasis, seborrheic dermatitis, and lichen simplex chronicus. The specimens of normal skin showed only weak basal layer staining with anti-interferon-gamma-induced protein 10. Thus, the presence of interferon-gamma-induced protein 10 in keratinocytes was associated with psoriasiform hyperplasia and could be detected in both AIDS-associated and classic psoriasis.
 ...
PMID:Detection of the interferon-gamma-induced protein 10 in psoriasiform dermatitis of acquired immunodeficiency syndrome. 214 26

A survey is given about the so far known mode of action and the therapeutic application of the following agents with immunostimulatory effects: Interleukin-2, Interferon-gamma, Tumor necrosis factor, Thymosin alpha 1, Thymopentin, Splenopentin, Thymulin, Thymostimulin, Muramyl dipeptide, Bestatin, Tuftsin and Levamisole. The treatment of patients suffering from immunodeficiency disorders and cancer with such agents seems to be possible in the near future.
 ...
PMID:[Immunostimulants--therapeutic aspects]. 249 78

Peripheral blood mononuclear cells (PBMCs) from many asymptomatic individuals infected with human immunodeficiency virus-type 1 (HIV) are unresponsive as measured by in vitro T cell proliferation and interleukin-2 (IL-2) production to influenza virus and synthetic peptides of HIV envelope (Env). Strong influenza virus- and Env-stimulated IL-2 responses and T cell proliferation were restored when cultures were stimulated in the presence of IL-12. Interferon-gamma production by PBMCs from HIV seropositive (HIV+) patients was also restored with IL-12. Furthermore, in vitro antigen-specific production of IL-2 and proliferation of PBMCs from HIV- donors were suppressed by antibody to IL-12, but were not enhanced by addition of exogenous IL-12. Thus, IL-12 may be limiting in PBMCs from HIV+ but not HIV- individuals. These findings demonstrate that IL-12 can restore HIV-specific cell-mediated immunity in vitro in HIV-infected individuals and suggest a potential use of IL-12 in augmenting the diminished immunologic functions associated with HIV infection.
 ...
PMID:Restoration of HIV-specific cell-mediated immune responses by interleukin-12 in vitro. 790 23

A murine acquired immunodeficiency syndrome (MAIDS) is induced in genetically susceptible strains of mice inoculated with LP-BM5 murine leukemia virus. It is characterized by progressive lymphoproliferation, profound immunodeficiency, and the subsequent loss of resistance to opportunistic pathogens, including intestinal pathogens. Cellular and/or humoral immunity of gut-associated lymphoid tissues may play a key role in the elimination of these pathogens. We have previously demonstrated reductions in the number of mucosal T and B cells in MAIDS. In this study, the cytokine production by mesenteric lymph nodes (MLN) cells and their proliferative response to mitogens during MAIDS were investigated. Alterations were observed in the kinetics of MLN cell proliferation and cytokine secretion by in vitro mitogen-stimulated MLN cells during the retrovirus infection. Cytokine production was abnormally changed, with a gradual decrease in interleukin-2 (IL-2) production as well as an increase in IL-5 and IL-6 secretion. Interferon-gamma production was increased during the progression to MAIDS. The dysregulated release of cytokines by MLN cells due to retrovirus infection could lead to immune dysfunction. These data indicate that dysregulated cytokine secretion by MLN cells may be responsible for impaired mucosal immunity in AIDS, explaining the dramatic increase of opportunistic intestinal pathogens in individuals with AIDS.
 ...
PMID:The kinetics of cytokine secretion and proliferation by mesenteric lymph node cells during the progression to murine AIDS, caused by LP-BM5 murine leukemia virus infection. 806 35

We investigated the effect of human immunodeficiency virus type 1 (HIV-1) recombinant gp120 (rec.gp120) on phenotype and function of cultured monocytes. Rec.gp120 significantly reduced the accessory function of monocytes to stimulate autologous lymphocytes with anti-CD3, the Fc receptor-mediated chemiluminescence of monocytes, and the expression of CD4 and Fc receptor I/II, while the expression of the monocyte marker CD14 and major histocompatibility complex class I and II was not influenced. According to these phenotypic results, preincubation of monocytes with rec.gp120 depressed anti-CD3 antibody-induced T cell stimulation and Fc receptor-mediated phagocytosis as determined by chemiluminescence. Interferon-gamma release of lymphocytes induced by purified protein derivative of tuberculin was enhanced by gp120. These effects of isolated gp120 on monocyte immune functions in vitro might contribute to the understanding of the pathophysiology of HIV-1 infection in vivo.
 ...
PMID:HIV-1 envelope protein gp120 affects phenotype and function of monocytes in vitro. 814 26

Interferon-gamma (IFN-gamma) had been shown to increase superoxide production of cultured monocytes from patients with chronic granulomatous disease (CGD). To elucidate the mechanism of the IFN-gamma-induced improvement of superoxide production of cultured monocytes from patients with CGD we examined the influence of IFN-gamma on the expression and the activity of the NADPH-oxidase in the monocytic cell-line Mono Mac 6. After cultivation of Mono Mac 6-cells in the presence of 500 U/ml IFN-gamma the superoxide production was found to be increased as well as the expression of the p47-phox cytosolic protein of the phagocytic NADPH-oxidase.
Immunodeficiency 1993
PMID:Is the IFN-gamma-induced enhancement of superoxide production in CGD-phagocytes caused by increased expression of the p47-phox cytosolic protein. 816 97

We examined the host defence mechanism against infection with Listeria monocytogenes, a facultative intracellular bacterium, in mice with murine acquired immunodeficiency syndrome (MAIDS) caused by LP-BM5 murine leukaemia virus (MuLv) infection. Although LP-BM5 MuLV infection in C57BL/6 mice leads to a stage of immunodeficiency characterized by severe compromise of cell-mediated immunity, the mice with established MAIDS infected with LP-BM5 8 weeks previously, showed resistance to an intraperitoneal infection with Listeria monocytogenes. These MAIDS mice also showed resistance to a lethal dose of secondary listerial challenge, while the delayed-type hypersensitivity response to heat-killed Listeria (HKL.) was severely impaired in MAIDS mice. The resistance of MAIDS mice to listerial infection was mediated by CD4+ alpha beta T cells but neither by gamma delta T cells nor natural killer (NK) cells. Interferon-gamma (IFN-gamma) and interleukin-10 (IL-10) were produced by CD4+ T cells from Listeria-infected MAIDS mice in response to the in vitro stimulation with HKL, whereas IFN-gamma but not IL-10 were produced by those from Listeria-infected control mice. These results suggest that T-helper 0 (Th0)-like immune responses of CD4+ T cells occur and participate in host defence mechanisms against listerial infection in MAIDS mice.
 ...
PMID:Th0-like CD4+ T cells protect mice with murine retrovirus-induced immunodeficiency syndrome (MAIDS) against co-infection with Listeria monocytogenes. 901 17


1 2 3 Next >>