Journal
LIPIDS
Volume 39, Issue 12, Pages 1163-1170Publisher
WILEY
DOI: 10.1007/s11745-004-1343-y
Keywords
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Funding
- NIDDK NIH HHS [DK53055] Funding Source: Medline
- NIEHS NIH HHS [P30-ES09106] Funding Source: Medline
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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 death-inducing 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.
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