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Journal ArticleDOI

CD4+ T Cell Clones Producing both Interferon-γ and Interleukin-10 Predominate in Bronchoalveolar Lavages of Active Pulmonary Tuberculosis Patients

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TLDR
The results indicate the predominance of CD4+ T cells producing both the pro inflammatory cytokine IFN-γ and the anti-inflammatory cytokine IL-10 in BAL of patients with active TB.
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This article is published in Clinical Immunology.The article was published on 1999-09-01. It has received 172 citations till now. The article focuses on the topics: T cell & CD8.

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Citations
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Journal ArticleDOI

Interleukin-10 and the interleukin-10 receptor.

TL;DR: Findings that have advanced the understanding of IL-10 and its receptor are highlighted, as well as its in vivo function in health and disease.
Journal ArticleDOI

The regulation of IL-10 production by immune cells

TL;DR: Understanding the specific molecular events that regulate the production of IL-10 will help to answer the remaining questions that are important for the design of new strategies of immune intervention.
Journal ArticleDOI

CD4 + CD25 + regulatory T cells control Leishmania major persistence and immunity

TL;DR: It is shown that the persistence of Leishmania major in the skin after healing in resistant C57BL/6 mice is controlled by an endogenous population of CD4+CD25+ regulatory T cells, indicating that the equilibrium established between effector and regulatory T Cells in sites of chronic infection might reflect both parasite and host survival strategies.
Journal ArticleDOI

The Immune Response in Tuberculosis

TL;DR: What the authors know about the immune response in tuberculosis, in human disease, and in a range of experimental models is summarized, all of which are essential to advancing the mechanistic knowledge base of the host-pathogen interactions that influence disease outcome.
Journal ArticleDOI

Natural Interferon α/β–Producing Cells Link Innate and Adaptive Immunity

TL;DR: Virus-activated IPCs may play two master roles in antiviral immune responses: directly inhibiting viral replication by producing large amounts of IFN-α/β, and subsequently triggering adaptive T cell–mediated immunity by differentiating into DCs.
References
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Journal ArticleDOI

Functional diversity of helper T lymphocytes.

TL;DR: The existence of subsets of CD4+ helper T lymphocytes that differ in their cytokine secretion patterns and effector functions provides a framework for understanding the heterogeneity of normal and pathological immune responses.
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A CD4 + T-cell subset inhibits antigen-specific T-cell responses and prevents colitis

TL;DR: It is shown that chronic activation of both human and murine CD4+T cells in the presence of interleukin (IL)-10 gives rise to CD4-T-cell clones with low proliferative capacity, producing high levels ofIL-10, low levels of IL-2 and no IL-4.
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Interleukin 10 (IL-10) and viral IL-10 strongly reduce antigen-specific human T cell proliferation by diminishing the antigen-presenting capacity of monocytes via downregulation of class II major histocompatibility complex expression.

TL;DR: It is indicated that IL-10 and v-IL-10 can completely prevent antigen-specific T cell proliferation by inhibition of the antigen-presenting capacity of monocytes through downregulation of class II MHC antigens on monocytes.
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Interleukin 10 (IL-10) inhibits human lymphocyte interferon gamma-production by suppressing natural killer cell stimulatory factor/IL-12 synthesis in accessory cells.

TL;DR: It is shown that IL-10 is a potent inhibitor of NKSF/IL-12 production from human peripheral blood mononuclear cells activated with Staphylococcus aureus or lipopolysaccharide (LPS), and that antibodies against NKSF-12, TNF-alpha, or IL-1 beta can significantly inhibit IFN-gamma production in response to various stimuli.
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A mutation in the interferon-gamma-receptor gene and susceptibility to mycobacterial infection.

TL;DR: Four children with severe mycobacterial infections had a mutation in the gene for interferon-gamma receptor 1 that leads to the absence of receptors on cell surfaces and a functional defect in the up-regulation of tumor necrosis factor alpha by macrophages in response to interferOn-Gamma.
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