Document Detail


n-3 polyunsaturated fatty acids suppress mitochondrial translocation to the immunologic synapse and modulate calcium signaling in T cells.
MedLine Citation:
PMID:  20393134     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Recent studies indicate that the process of Ag presentation induces cytoskeleton-dependent mitochondrial redistribution to the immediate vicinity of the immunologic synapse (IS). This redistribution of mitochondria to the IS in T cells is necessary to maintain Ca(2+) influx and Th cell activation. Recently, we demonstrated that n-3 polyunsaturated fatty acids (PUFAs) suppress the localization and activation of signaling proteins at the IS. Therefore, we hypothesized that n-3 PUFAs suppress CD4(+) T cell mitochondrial translocation during the early stages of IS formation and downmodulate Ca(2+)-dependent Th cell activation. CD4(+) cells derived from fat-1 mice, a transgenic model that synthesizes n-3 PUFA from n-6 PUFA, were cocultured with anti-CD3-expressing hybridoma cells (145-2C11) for 15 min at 37 degrees C, and mitochondrial translocation to the IS was assessed by confocal microscopy. Fat-1 mice exhibited a significantly (p < 0.05) reduced percentage of T cells with mitochondria which translocated to the IS; fat-1 (30%) versus wild type control (82%). Regarding the effect on the mitochondrial-to-cytosolic Ca(2+) ratio, wild type cells showed significant increases at the IS (71%) and total cell (60%) within 30 min of IS formation. In contrast, fat-1 CD4(+) T cells remained at basal levels following the IS formation. A similar blunting of the mitochondrial-to-cytosolic Ca(2+) ratio was observed in wild type cells that were coincubated with inhibitors of the mitochondrial uniporter, RU360 or calcium release-activated Ca(2+) (CRAC) channels, BTP2. These observations provide evidence that n-3 PUFAs modulate Th cell activation by limiting mitochondrial translocation to the IS and reducing Ca(2+) entry.
Authors:
Rajeshwari Yog; Rola Barhoumi; David N McMurray; Robert S Chapkin
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2010-04-14
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  184     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2010 May 
Date Detail:
Created Date:  2010-05-20     Completed Date:  2010-07-19     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  5865-73     Citation Subset:  AIM; IM    
Affiliation:
Department of Veterinary Integrative Biosciences.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigen-Presenting Cells / cytology,  immunology,  metabolism
CD4-Positive T-Lymphocytes / cytology,  immunology*,  metabolism*
Calcium Signaling / immunology*
Cell Communication / immunology
Coculture Techniques
Fatty Acids, Omega-3 / physiology*
Hybridomas
Immune Tolerance
Immunological Synapses / immunology*,  metabolism*
Lymphocyte Activation / immunology
Mice
Mice, Inbred C57BL
Mice, Transgenic
Mitochondrial Proteins / physiology*
Protein Transport / immunology
Grant Support
ID/Acronym/Agency:
1 S10 RR22532-01/RR/NCRR NIH HHS; DK 071707/DK/NIDDK NIH HHS; P30ES09106/ES/NIEHS NIH HHS
Chemical
Reg. No./Substance:
0/Fatty Acids, Omega-3; 0/Mitochondrial Proteins

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