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Effects of dietary n−3 polyunsaturated fatty acids on T‐Cell membrane composition and function
Author(s) -
Switzer Kirsten C.,
McMurray David N.,
Chapkin Robert S.
Publication year - 2004
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/s11745-004-1343-y
Subject(s) - lipid raft , microbiology and biotechnology , signal transduction , inflammation , polyunsaturated fatty acid , biology , apoptosis , t cell , cell growth , cell , programmed cell death , biochemistry , immunology , immune system , fatty acid
Dietary n−3 PUFA have been shown to attenuate T‐cell‐mediated inflammation, in part, by suppressing T‐cell activation and proliferation. n−3 PUFA have also been shown to promote apoptosis, another important mechanism for the prevention of chronic inflammation by maintaining T‐cell homeostasis through the contraction of populations of activated T cells. Recent studies have specifically examined Fas death receptor‐mediated activation‐induced cell death (AICD), since it is the form of apoptosis associated with peripheral T‐cell deletion involved in immunological tolerance and T‐cell homeostasis. Data from our laboratory indicate that n−3 PUFA promote AICD in T helper 1 polarized cells, which are the mediators of chronic inflammation. Since Fas and components of the deathinducing signaling complex are recruited to plasma membrane microdomains (rafts), the effect of dietary n−3 PUFA on raft composition and resident protein localization has been the focus of recent investigations. Indeed, there is now compelling evidence that dietary n−3 PUFA are capable of modifying the composition of T‐cell membrane microdomains (rafts). Because the lipids found in membrane microdomains actively participate in signal transduction pathways, these results support the hypothesis that dietary n−3 PUFA influence signaling complexes and modulate T‐cell cytokinetics in vivo by altering T‐cell raft composition.