NDLI: Monocyte-derived IL-5 reduces TNF production by Mycobacterium tuberculosis-specific CD4 T cells during SIV/M. tuberculosis coinfection.

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Protective role of the inflammatory CCR2/CCL2 chemokine pathway through recruitment of type 1 cytotoxic Î³Î´ T lymphocytes to tumor beds.

Reciprocal negative cross-talk between liver X receptors (LXRs) and STAT1: effects on IFN-Î³-induced inflammatory responses and LXR-dependent gene expression.

Recent thymic emigrants and mature naive T cells exhibit differential DNA methylation at key cytokine loci.

Helicobacter pylori infection inhibits phagocyte clearance of apoptotic gastric epithelial cells.

Antigen-specific effector CD4 T lymphocytes school lamina propria dendritic cells to transfer innate tolerance.

CD40 mediates downregulation of CD32B on specific memory B cell populations in rheumatoid arthritis.

GB virus C particles inhibit T cell activation via envelope E2 protein-mediated inhibition of TCR signaling.

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MicroRNA-155 confers encephalogenic potential to Th17 cells by promoting effector gene expression.

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Monocyte-derived IL-5 reduces TNF production by Mycobacterium tuberculosis-specific CD4 T cells during SIV/M. tuberculosis coinfection.

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Metabolic adaptation of neutrophils in cystic fibrosis airways involves distinct shifts in nutrient transporter expression.

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Transglutaminase 2-specific autoantibodies in celiac disease target clustered, N-terminal epitopes not displayed on the surface of cells.

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T cell costimulation with anti-CD137 monoclonal antibodies is mediated by K63-polyubiquitin-dependent signals from endosomes.

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Comment on 'TLR9 provokes inflammation in response to fetal DNA: mechanism for fetal loss in preterm birth and preeclampsia'.

Comment on 'Induced IL-17-producing invariant NKT cells require activation in presence of TGF-ß and IL-1ß'.

Response to comment on 'Induced IL-17-producing invariant NKT cells require activation in presence of TGF-ß and IL-1ß'.

What is and what should always have been: long-lived plasma cells induced by T cell-independent antigens.

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Monocyte-derived IL-5 reduces TNF production by Mycobacterium tuberculosis-specific CD4 T cells during SIV/M. tuberculosis coinfection.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Mattila, Joshua T. Flynn, JoAnne L. Diedrich, Collin R.
Description	Country affiliation: United States Author Affiliation: Diedrich CR ( Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.)
Abstract	HIV-infected individuals are significantly more susceptible to tuberculosis (TB) than uninfected individuals. Although it is established that HIV reduces Mycobacterium tuberculosis-specific T cell responses, the causes of this dysfunction are not known. We used the cynomolgus macaque model of TB to demonstrate that ex vivo SIV reduces the frequency of M. tuberculosis-specific TNF and IFN-Î³-producing T cells within 24 h after infection. In vivo, T cell IFN-Î³ responses in granulomas from animals with SIV/M. tuberculosis coinfection were lower than SIV-negative animals with active TB. The SIV effects on the inhibition of T cell responses were primarily on APCs and not the T cells directly. Specifically, reductions in the frequency of TNF-producing M. tuberculosis-specific CD4 T cells were caused, at least in part, by SIV-induced production of monocyte derived IL-5.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1202043
Journal	The Journal of Immunology
Issue Number	12
Volume Number	190
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-06-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cd4-positive T-lymphocytes Immunology Interleukin-5 Metabolism Monocytes Simian Acquired Immunodeficiency Syndrome Complications Tuberculosis Tumor Necrosis Factor-alpha Biosynthesis Animals Cell Separation Flow Cytometry Macaca Fascicularis Mycobacterium Tuberculosis Reverse Transcriptase Polymerase Chain Reaction Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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