NDLI: Defective T cell development and function in calcineurin Aβ-deficient mice

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Defective T cell development and function in calcineurin Aβ-deficient mice

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Defective T cell development and function in calcineurin Aβ-deficient mice

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Molkentin, Jeffery D. Rothenberg, Marc E. Brandt, Eric B. Bueno, Orlando F.
Description	Author Affiliation: Bueno OF ( Division of Molecular Cardiovascular Biology, Department of Pediatrics, Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229-3039, USA.);
Abstract	The calcium-dependent phosphatase calcineurin and its downstream transcriptional effector nuclear factor of activated T cells (NFAT) are important regulators of inducible gene expression in multiple cell types. In T cells, calcineurin-NFAT signaling represents a critical event for mediating cellular activation and the immune response. The widely used immunosuppressant agents cyclosporin and FK506 are thought to antagonize the immune response by directly inhibiting calcineurin-NFAT signal transduction in lymphocytes. To unequivocally establish the importance of calcineurin signaling as a mediator of the immune response, we deleted the gene encoding the predominant calcineurin isoform expressed in lymphocytes, calcineurin A beta (CnA beta). CnA beta(-/-) mice were viable as adults, but displayed defective T cell development characterized by fewer total CD3 cells and reduced CD4 and CD8 single positive cells. Total peripheral T cell numbers were significantly reduced in CnA beta(-/-) mice and were defective in proliferative capacity and IL-2 production in response to PMA/ionomycin and T cell receptor cross-linking. CnA beta(-/-) mice also were permissive to allogeneic tumor-cell transplantation in vivo, similar to cyclosporin-treated wild-type mice. A mechanism for the compromised immune response is suggested by the observation that CnA beta(-/-) T cells are defective in stimulation-induced NFATc1, NFATc2, and NFATc3 activation. These results establish a critical role for CnA beta signaling in regulating T cell development and activation in vivo.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	14
Volume Number	99
Language	English
Publisher	National Academy of Sciences
Publisher Date	2002-07-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Calcineurin Deficiency Nuclear Proteins T-Lymphocytes Immunology Animals Genetics Physiology Cytotoxicity, Immunologic DNA-Binding Proteins Metabolism In Vitro Techniques Interleukin-2 Biosynthesis Ionomycin Pharmacology Lymphocyte Activation Mice Mice, Inbred C57BL Mice, Knockout NFATC Transcription Factors Plasmacytoma Receptors, Antigen, T-Cell Signal Transduction Drug Effects Tetradecanoylphorbol Acetate Transcription Factors Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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