NDLI: The importance of the Erk pathway in the development of linker for activation of T cells-mediated autoimmunity.

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The importance of the Erk pathway in the development of linker for activation of T cells-mediated autoimmunity.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Koonpaew, Surapong Fuller, Deirdre M. Nelson, Mariana I. Zhu, Minghua Zhang, Weiguo
Description	Country affiliation: United States Author Affiliation: Fuller DM ( Department of Immunology, Duke University Medical Center, Durham, NC 27710, USA.)
Abstract	The ability of the transmembrane adaptor protein linker for activation of T cells (LAT) to regulate T cell development, activation, survival, and homeostasis depends upon phosphorylation of its multiple tyrosine residues. The mutation of tyrosine 136 on LAT abrogates its interaction with phospholipase C-Î³1, causing severe ramifications on TCR-mediated signaling. Mice harboring this mutation, LATY136F mice, have significantly impaired thymocyte development; however, they rapidly develop a fatal lymphoproliferative disease marked by the uncontrolled expansion of Th2-skewed CD4(+) T cells, high levels of IgE and IgG1, and autoantibody production. In this study, we assessed the contribution of multiple signaling pathways in LATY136F disease development. The deletion of the critical signaling proteins Gads and RasGRP1 caused a further block in thymocyte development, but, over time, could not prevent CD4(+) T cell hyperproliferation. Also, restoring signaling through the NF-κB and NFAT pathways was unable to halt the development of disease. However, expression of a constitutively active Raf transgene enhanced lymphoproliferation, indicating a role for the Ras-MAPK pathway in LAT-mediated disease.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1201380
Journal	The Journal of Immunology
Issue Number	8
Volume Number	189
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-10-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Adaptor Proteins, Signal Transducing Physiology Autoimmune Diseases Enzymology Immunology Lymphoproliferative Disorders Map Kinase Signaling System Membrane Proteins Phosphoproteins Deficiency Genetics Animals Guanine Nucleotide Exchange Factors Mice Mice, Knockout Mice, Transgenic Receptors, Antigen, T-cell Raf Kinases Biosynthesis Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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A phospholipase C-Î³1-independent, RasGRP1-ERK-dependent pathway drives lymphoproliferative disease in linker for activation of T cells-Y136F mutant mice.

Catalytic activity of the mouse guanine nucleotide exchanger mSOS is activated by Fyn tyrosine protein kinase and the T-cell antigen receptor in T cells.

The Importance of IL-6 in the Development of LAT-Mediated Autoimmunity.

The requirement of linker for activation of T cells in the primary and memory responses of CD8 T cells.

Homeostatic division is not necessary for antigen-specific CD4+ memory T cell persistence.

STAT6 deletion converts the Th2 inflammatory pathology afflicting Lat(Y136F) mice into a lymphoproliferative disorder involving Th1 and CD8 effector T cells.

Distinct regulation of integrin-dependent T cell conjugate formation and NF-kappa B activation by the adapter protein ADAP.

Essential role of Elmo1 in Dock2-dependent lymphocyte migration.

B-cell linker protein expression contributes to controlling allergic and autoimmune diseases by mediating IL-10 production in regulatory B cells.

The importance of the Erk pathway in the development of linker for activation of T cells-mediated autoimmunity.

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