Polyunsaturated fatty acids interfere with formation of the immunological synapse (original) (raw)
Journal Article
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Department of Internal Medicine III, Medical University of Vienna
,
Austria
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Department of Internal Medicine III, Medical University of Vienna
,
Austria
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Institute of Immunology, Medical University of Vienna
,
Austria
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Department of Internal Medicine III, Medical University of Vienna
,
Austria
CeMM-Center of Molecular Medicine of the Austrian Academy of Sciences
, Vienna
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Department of Internal Medicine III, Medical University of Vienna
,
Austria
CeMM-Center of Molecular Medicine of the Austrian Academy of Sciences
, Vienna
Correspondence: Department of Internal Medicine III, Medical University of Vienna, Währinger Gürtel 18-20, A-1090 Vienna, Austria. E-mail: thomas.stulnig@meduniwien.ac.at
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Received:
25 November 2004
Revision received:
27 December 2004
Accepted:
16 January 2005
Published:
09 February 2005
Cite
René Geyeregger, Maximilian Zeyda, Gerhard J Zlabinger, Werner Waldhäusl, Thomas M Stulnig, Polyunsaturated fatty acids interfere with formation of the immunological synapse, Journal of Leukocyte Biology, Volume 77, Issue 5, May 2005, Pages 680–688, https://doi.org/10.1189/jlb.1104687
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Abstract
Polyunsaturated fatty acids (PUAs) exert inhibitory effects on T cell-mediated immune responses. Activation of T cells in vivo depends on formation of an immunological synapse (IS) at the T cell/antigen-presenting cell (APC) interface. Here, we analyzed effects of PUFA treatment on the formation of the IS and APC-induced human T cell activation. In T cells treated with the PUFA eicosapentaenoic (EPA; 20:5,n-3) and arachidonic acid (20:4,n-6), stimulated by superantigen-presenting cells or APCs, relocalization to the IS of distinct molecules [F-actin, talin, leukocyte functional antigen-1α, clusters of differentiation (CD)3ɛ] was inhibited markedly compared with cells treated with saturated fatty acid, whereas relocalization of protein kinase Cθ to the IS remained unaffected. CD3-induced, sustained phosphorylation of nucleotide exchange factor Vav, which controls cytoskeletal rearrangements underlying IS formation, was significantly reduced in EPA-treated Jurkat and peripheral blood T cells. In addition, T cell raft disruption by methyl-β-cyclodextrin treatment and experiments with a chimeric linker for activation of T cell proteins, which is resistant to PUFA effects on lipid rafts, revealed modifications of lipid rafts as a crucial factor for PUFA-mediated inhibition of APC-stimulated cytoskeletal rearrangements. Furthermore, the efficiency of T cell/APC conjugate formation was significantly reduced with EPA-treated T cells, as was stimulation of CD69 expression, which is not altered following antibody-mediated T cell activation. In conclusion, PUFA treatment of T cells qualitatively and quantitatively alters IS formation, thereby extending T cell signaling defects to pathways that are not intrinsically altered in PUFA-treated T cells when stimulated by antibodies.
© 2005 Society for Leukocyte Biology
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