NDLI: Viral antigen induces differentiation of Foxp3+ natural regulatory T cells in influenza virus-infected mice.

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STAT4-dependent and -independent Th2 responses correlate with protective immunity against lung infection with Pneumocystis murina.

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Viral antigen induces differentiation of Foxp3+ natural regulatory T cells in influenza virus-infected mice.

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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.

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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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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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Viral antigen induces differentiation of Foxp3+ natural regulatory T cells in influenza virus-infected mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zakhary, Nardine Garlick, David S. Garcia, Victoria Weissler, Katherine Leibow, Abigail Kropf, Elizabeth Bedoya, Felipe Cheng, Guang-Shing Aitken, Malinda Wherry, E. John Erikson, Jan Caton, Andrew J.
Description	Country affiliation: United States Author Affiliation: Bedoya F ( The Wistar Institute, Philadelphia, PA 19104, USA.)
Abstract	We examined the formation, participation, and functional specialization of virus-reactive Foxp3(+) regulatory T cells (Tregs) in a mouse model of influenza virus infection. 'Natural' Tregs generated intrathymically, based on interactions with a self-peptide, proliferated in response to a homologous viral Ag in the lungs and, to a lesser extent, in the lung-draining mediastinal lymph nodes (medLNs) of virus-infected mice. In contrast, conventional CD4(+) T cells with identical TCR specificity underwent little or no conversion to become 'adaptive' Tregs. The virus-reactive Tregs in the medLNs and the lungs of infected mice upregulated a variety of molecules associated with Treg activation, as well as acquired expression of molecules (T-bet, Blimp-1, and IL-10) that confer functional specialization to Tregs. Notably, however, the phenotypes of the T-bet(+) Tregs obtained from these sites were distinct, because Tregs isolated from the lungs expressed significantly higher levels of T-bet, Blimp-1, and IL-10 than did Tregs from the medLNs. Adoptive transfer of Ag-reactive Tregs led to decreased proliferation of antiviral CD4(+) and CD8(+) effector T cells in the lungs of infected hosts, whereas depletion of Tregs had a reciprocal effect. These studies demonstrate that thymically generated Tregs can become activated by a pathogen-derived peptide and acquire discrete T-bet(+) Treg phenotypes while participating in and modulating an antiviral immune response.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1203302
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	Lymphocyte Activation Immunology Orthomyxoviridae Infections T-lymphocyte Subsets T-lymphocytes, Regulatory Adoptive Transfer Animals Antigens, Viral Cell Differentiation Flow Cytometry Forkhead Transcription Factors Mice Mice, Inbred Balb C Mice, Transgenic Orthomyxoviridae Phenotype Real-time Polymerase Chain Reaction Reverse Transcriptase Polymerase Chain Reaction Cytology Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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