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Frequent detection and isolation of cytopathic retroviruses (HTLV-III) from patients with AIDS and at risk for AIDS.
Peripheral blood lymphocytes from patients with the acquired immunodeficiency syndrome (AIDS) or with signs or symptoms that frequently precede AIDS (pre-AIDS) were grown in vitro with added T-cell…
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Stat6 is required for mediating responses to IL-4 and for development of Th2 cells.
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The role of mononuclear phagocytes in HTLV-III/LAV infection.
TLDR
It is suggested that mononuclear phagocytes may serve as primary targets for infection and agents for virus dissemination and that these virus-infected cells may play a role in the pathogenesis of the disease.
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Impaired IL-12 responses and enhanced development of Th2 cells in Stat4-deficient mice
TLDR
It is demonstrated that Stat4 is essential for mediating responses to IL-12 in lymphocytes, and regulating the differentiation of both Th1 and Th2 cells.
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Stat3 and Stat4 Direct Development of IL-17-Secreting Th Cells1
TLDR
It is demonstrated that Stat3 is required for programming the TGFβ1 plus IL-6 and IL-23-stimulated IL-17-secreting phenotype, as well as for RORγt expression in TGF β1 plusIL-6-primed cells.
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Isolation of a new virus, HBLV, in patients with lymphoproliferative disorders.
TLDR
A novel human B-lymphotropic virus (HBLV) was isolated from the peripheral blood leukocytes of six individuals and selectively infected freshly isolated human B cells and converted them into large, refractile mono- or binucleated cells with nuclear and cytoplasmic inclusion bodies.
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The transcription factor PU.1 is required for the development of interleukin 9-producing T cells and allergic inflammation
TLDR
A critical role is suggested in generating the IL-9-producing (TH9) phenotype and in the development of allergic inflammation in mice with PU.1-deficient T cells, which corresponds to lower expression of Il9 and chemokines in peripheral T cells and in lungs than that of wild-type mice.
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Signal transducer and activator of transcription 4 is required for the transcription factor T-bet to promote T helper 1 cell-fate determination.
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Interferon regulatory factor 4 sustains CD8(+) T cell expansion and effector differentiation.
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STAT5 programs a distinct subset of GM-CSF-producing T helper cells that is essential for autoimmune neuroinflammation
TLDR
The results showed that loss of encephalitogenic activity of STAT5-deficient autoreactive CD4+ T cells was independent of IFN-γ or interleukin 17 (IL-17) production, but was due to the impaired expression of granulocyte-macrophage colony-stimulating factor (GM-CSF), a crucial mediator of T-cell pathogenicity.
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