NDLI: Polar opposites: Erk direction of CD4 T cell subsets.

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Polar opposites: Erk direction of CD4 T cell subsets.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Ch'en, Irene L. D'Souza, Warren N. Pages, Gilles Chang, Chiung-Fang Hedrick, Stephen M. Pouyssegur, Jacques
Description	Country affiliation: United States Author Affiliation: Chang CF ( University of California, San Diego, La Jolla, CA 92093-0377, USA.)
Abstract	Effective immune responses depend upon appropriate T cell differentiation in accord with the nature of an infectious agent, and the contingency of differentiation depends minimally on TCR, coreceptor, and cytokine signals. In this reverse genetic study, we show that the MAPK Erk2 is not essential for T cell proliferation in the presence of optimum costimulation. Instead, it has opposite effects on T-bet and Gata3 expression and, hence, on Th1 and Th2 differentiation. Alternatively, in the presence of TGF-ß, the Erk pathway suppresses a large program of gene expression, effectively limiting the differentiation of Foxp3(+) regulatory T cells. In the latter case, the mechanisms involved include suppression of Gata3 and Foxp3, induction of Tbx21, phosphorylation of Smad2,3, and possibly suppression of Socs2, a positive inducer of Stat5 signaling. Consequently, loss of Erk2 severely impeded Th1 differentiation while enhancing the development of Foxp3(+)-induced T regulatory cells. Selected profiles of gene expression under multiple conditions of T cell activation illustrate the opposing consequences of Erk pathway signaling.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1103015
Journal	The Journal of Immunology
Issue Number	2
Volume Number	189
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-07-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cd4-positive T-lymphocytes Enzymology Immunology Cell Polarity Mitogen-activated Protein Kinase 1 Physiology T-lymphocyte Subsets Animals Virology Cell Differentiation Genetics Cell Proliferation Cells, Cultured Forkhead Transcription Factors Biosynthesis Lymphocytic Choriomeningitis Virus Mice Mice, Knockout Mice, Transgenic Deficiency T-lymphocytes, Regulatory Th1 Cells Up-regulation Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Differential T cell responses to residual viral antigen prolong CD4+ T cell contraction following the resolution of infection.

FoxO1 controls effector-to-memory transition and maintenance of functional CD8 T cell memory.

MyD88 plays a critical T cell-intrinsic role in supporting CD8 T cell expansion during acute lymphocytic choriomeningitis virus infection.

Polar opposites: Erk direction of CD4 T cell subsets 1

B cell depletion curtails CD4+ T cell memory and reduces protection against disseminating virus infection.

IFN-λ exerts opposing effects on T cell responses depending on the chronicity of the virus infection.

Protein energy malnutrition impairs homeostatic proliferation of memory CD8 T cells.

CD70 deficiency impairs effector CD8 T cell generation and viral clearance but is dispensable for the recall response to lymphocytic choriomeningitis virus.

Polar opposites: Erk direction of CD4 T cell subsets.

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Polar opposites: Erk direction of CD4 T cell subsets.