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Query: UMLS:C0021311 (Infection)
 38,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Continuous cultivation of peripheral blood lymphocytes from healthy sheep was carried out in vitro with the help of human recombinant interleukin-2. Lymphocytes were concurrently cultivated with the lethally X-rayed BLV-producing FLK culture cells. Electron microscopy and dot-blot hybridization established that sheep peripheral blood lymphocytes were infected with BLV and a full cycle of replication takes place in them. Infection of sheep leukocytes in vitro can be used to study the mechanisms of leukogenesis in vitro.
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PMID:[Infection of peripheral blood lymphocytes in sheep with bovine leukemia virus in vitro]. 254 21

The phenotype and functions of T lymphocytes and of natural killer (NK) cells have been investigated in four children and five adults from three Italian families infected with HIV (LAV/HTLV III). The results show a heterogeneous pattern of immunological derangements involving distribution of T and natural killer subsets, proliferation in response to T cell mitogens and natural killer activity. However, all infected patients tested showed a very low or absent phytohaemagglutinin induced interleukin-2 production regardless of age and clinical conditions, while concanavalin A-induced interleukin-2 production was within the normal range. The impaired interleukin-2 production in response to phytohaemagglutinin in some patients is not related to phytohaemagglutinin-induced proliferation, to clinical conditions or to a defective distribution of T cell subsets. These results suggest that, in our patients, both adults and children, HIV (LAV/HTLV III) has an "early" tropism for a subset of T cells involved in interleukin-2 production.
Infection
PMID:Acquired immune deficiency syndrome in childhood: impaired production of interleukin-2 by HIV (LAV/HTLV III) infected patients. 295 15

Infection of human T cells by human T-lymphotropic virus, type I (HTLV-I), a retrovirus, is uniformly associated with the constitutive expression of large numbers of cellular receptors for interleukin-2 (IL-2). Comparison with normal T cells shows that neither IL-2 receptor gene organization nor IL-2 receptor messenger RNA processing are altered in the leukemic cells. However, mitogenic stimuli activate IL-2 receptor gene expression in normal T cells, whereas these stimuli paradoxically inhibit IL-2 receptor gene transcription in HTLV-I-infected leukemic T cells.
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PMID:Deregulation of interleukin-2 receptor gene expression in HTLV-I-induced adult T-cell leukemia. 298 27

Infection of normal peripheral blood T cells by the acquired immune deficiency syndrome (AIDS)-associated retrovirus (ARV) was evaluated in long-term cultures of helper-inducer T cells (T4 cells). Cells that were inoculated with ARV and maintained in medium supplemented with interleukin-2 remained productively infected with this virus for more than 4 months in culture, although they showed no cytopathic effects characteristic of acute ARV infection. The presence of replicating virus was demonstrated by reverse transcriptase activity of culture fluids and by viral antigens and budding particles detected on cells by immunofluorescence and electron microscopy. Virus produced in these cultures remained infectious and could induce cytopathic effects and viral antigens in uninfected lymphoid cells. The finding that normal lymphocytes may be productively infected by an AIDS retrovirus in the absence of cell death suggests that a range of biologic effects may occur after infection in vivo.
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PMID:Persistent noncytopathic infection of normal human T lymphocytes with AIDS-associated retrovirus. 299 22

Human T-cell leukemia virus type I (HTLV-I) encodes a trans-activator protein p40x which positively regulates transcription of the viral RNA as well as interleukin-2 and its receptor genes. We placed a cDNA coding for p40x in baculovirus Bombyx mori nuclear polyhedrosis virus (BmNPV) expression vectors. Infection of BmN cells derived from an insect, B. mori (silkworm), with a recombinant virus led to the production of soluble p40x. The biological activity of the recombinant p40x was demonstrated by introducing the protein into intact NIH 3T3 cells that had been selected for genomic integration of HTLV-I LTR connected with the CAT gene. Immunocytochemical and cell fractionation analyses showed the localization of p40x in both the cytoplasmic and nuclear fractions of BmN cells. Analyses of 32P-labeled proteins of BmN cells by cell fractionation and subsequent immunoprecipitation revealed that the p40x present in each subcellular fraction was phosphorylated. The post-translational modification was inhibited by the addition of a protein kinase inhibitor K252a during the metabolic labeling of BmN cells. Phosphoamino acid analysis indicated that the phosphorylation occurred on serine residues of p40x.
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PMID:Evidence for phosphorylation of trans-activator p40x of human T-cell leukemia virus type I produced in insect cells with a baculovirus expression vector. 305 77

Evidence is summarized to suggest that both CD4 and CD8 T cells and both helper and cytolytic T cell functions are involved in protective immunity to infection with the intracellular bacterium, Listeria monocytogenes. This suggestion is based on the following findings obtained with T cell lines and clones from L. monocytogenes infected mice: L3T4+ (CD4) T cells produce multiple lymphokines after antigen stimulation in vitro; Lyt2+ (CD8) T cells lyse L. monocytogenes primed macrophages; L3T4+ (CD4) T cells also lyse L. monocytogenes primed macrophages provided the latter express Ia-molecules; Lyt2+ (CD8) T cells secret Interferon-gamma provided that exogenous Interleukin-2 is supplied. Furthermore, both L3T4+ (CD4) and Lyt2+ (CD8) T cell lines can confer a certain degree of adoptive protection upon naive recipient mice.
Infection 1988
PMID:Listeria monocytogenes specific T-cell lines and clones. 313 85

Infection of CMS5 tumor cells with retroviral constructs containing interleukin-2 (IL-2) cDNA and selection in medium supplemented with G418 resulted in the isolation of clones which secreted IL-2. Whereas injection of parental tumor cells resulted in progressive tumor growth, tumor cells secreting high levels of IL-2 were rejected. Furthermore, in animals vaccinated with IL-2-secreting cells, the immunosuppression associated with the inoculation of parental tumor cells did not develop, and these animals resisted a challenge with viable tumor cells. To better understand the functional differences in the anti-tumor responses of immune and tumor-bearing mice which are at the basis for these diverse responses, we used an in vitro model to analyze interactions between splenic lymphocytes and tumor cells. Spleen cells isolated from either tumor-bearing or immune mice proliferated vigorously when cultured alone for 6 days, but much less in the presence of parental tumor cells. This effect could not be transferred with supernatant from tumor cell lines. Spleen cells from tumor-bearing mice remained unresponsive, while those from immune mice proliferated well in response to IL-2-secreting tumor cells. Only spleen cells from immune animals were able to develop cytotoxicity against CMS5 cells following in vitro restimulation. These results are consistent with the interpretation that exposure to parental tumor cells inhibited cell-mediated anti-tumor responses by a mechanism that involved cell-to-cell contact.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vaccination with IL-2-secreting tumor cells stimulates the generation of IL-2-responsive T cells and prevents the development of unresponsiveness. 762 Dec 37

Feline immunodeficiency virus (FIV) infection in the cat is similar to human immunodeficiency virus type 1 infection in causing a selective reduction in CD4+ cell numbers, leading to inversion of the CD4+/CD8+ ratio. To determine whether FIV, similar to human immunodeficiency virus type 1, has a tropism for CD4+ cells, we examined the in vitro and in vivo susceptibilities of feline lymphocyte subpopulations to FIV infection. Infection of interleukin-2-dependent CD4+ or CD8+ lymphocyte cultures with the NCSU1 isolate of FIV (FIV-NCSU1) resulted in syncytium formation, cell death, and Mg(2+)-dependent reverse transcriptase (RT) activity in both cases. Monoclonal antibodies to feline lymphocyte subsets were used to sort peripheral blood mononuclear cells from FIV-infected cats into highly (> 95%) purified CD4+ cell, CD8+ cell, immunoglobulin-positive (Ig+) cell, and monocyte subpopulations. The mononuclear cell subpopulations were analyzed for FIV provirus by polymerase chain reaction and Southern blot analysis and for virus expression by RT activity. All 16 cats infected with FIV-NCSU1 demonstrated FIV provirus in CD4+ cell-, CD8+ cell-, and Ig+ cell-enriched lymphocyte populations. Southern blot detection of amplified gag gene sequences and limiting-cell-dilution polymerase chain reaction analysis indicated that Ig+ cells carried a higher FIV provirus burden in chronically (> or = 1-year) infected cats than either CD4+ or CD8+ cells. In contrast, CD4+ cells carried the greatest provirus burden in acutely (2- to 4-week) infected cats. FIV provirus was detected in monocytes from only 1 of 10 cats with asymptomatic infection. Addition of culture supernatants from enriched CD4+, CD8+, and Ig+ cells from FIV-infected cats to an FIV-susceptible CD4+ lymphocyte culture resulted in syncytium formation, cell death, and RT activity. Infection of Ig+ cells is not unique to FIV-NCSU1, as lymphocyte subpopulations from other cats with natural infections and cats infected with the Petaluma or Mount Airy isolate of FIV demonstrated a similar distribution of FIV provirus and RT activity. These data suggest that FIV possesses a broad tropism for peripheral blood mononuclear cells and that an Ig+ cell may serve as a major reservoir for the virus in chronically infected cats.
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PMID:In vivo lymphocyte tropism of feline immunodeficiency virus. 768 19

Distinct patterns of T cell cytokine production have been shown to influence the outcome of infection in mouse models and humans. Th1 or Type 1 cytokines, interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) are generally associated with resistance to infection, whereas Th2 or Type 2 cytokines, IL-4 and IL-10 are associated with progressive disease. Leprosy is a useful model for studying the role of cytokines in modulating T cell responses in human infectious disease. Infection by Mycobacterium leprae results in disease manifestations that encompass an immunological spectrum. Tuberculoid patients are able to restrict the growth of the pathogen and mount strong T cell responses to M. leprae. In contrast, lepromatous patients manifest disseminated infection and their T cells weakly respond to M. leprae. We have found that tuberculoid leprosy lesions have a predominance of CD4+ T cells producing the Type 1 cytokine pattern. Secondly, IL-12 mRNA was expressed at 10-fold higher levels in tuberculoid lesions as compared to lepromatous lesions and that IL-12 promotes the selective expansion of the Type 1 cytokine producing cells. In contrast, lepromatous lesions contain CD8+ IL-4-producing cells that suppress antigen-specific T cell responses and promote the outgrowth of additional suppressor T cells. IL-10, also expressed at higher levels in lepromatous as compared to tuberculoid lesions, was found to be produced by macrophages, effectively inhibiting cytokine production and macrophage activity.
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PMID:Cytokine patterns at the site of mycobacterial infection. 771 51

Infection of mice with the protozoan parasite Leishmania major is an established model with which to study the in vivo development of CD4+ Th cell subsets. Interferon-gamma (IFN-gamma), produced by natural killer (NK) cells (AsGM1+, CD4-, CD8-, CD3-), regulates CD4+ T cell subset development and early resistance to L. major. Rapid Th1 cell development and resistance to infection occur in mice that develop an NK cell response early after infection (C3H and immunized BALB/c mice), whereas mice that lack an early NK cell response demonstrate delayed Th1 cell development and enhanced early disease (C57BL/6) or lack detectable Th1 cell development altogether and develop a progressive, fatal infection (BALB/c). Analysis of the requirements for NK cell activation in C3H mice revealed that the NK cell response is both interleukin-2 (IL-2) and IL-12 dependent. Although delayed IL-12 production in C57BL/6 mice precludes NK cell activation, the eventual development of a Th1 response appears to be IL-12 dependent. In contrast, concomitant production of inhibitory factors (IL-4, IL-10, and transforming growth factor beta) with IL-12 and IL-2 prevents NK cell activation in BALB/c mice. Together, these observations support a paradigm of in vivo Th1 cell development that involves IL-12-dependent stimulation of IFN-gamma production by NK cells.
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PMID:The role of the innate immune response in Th1 cell development following Leishmania major infection. 772 8


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