T cells respond to heat shock protein 60 via TLR2: activation of adhesion and inhibition of chemokine receptors
- 3 June 2003
- journal article
- retracted article
- Published by Wiley in The FASEB Journal
- Vol. 17 (11) , 1-21
- https://doi.org/10.1096/fj.02-1139fje
Abstract
SPECIFIC AIMSThe mammalian 60 kDa heat shock protein (HSP60) is a molecule of many facets. Besides serving as a chaperone, HSP60 is expressed by cells exposed to stress or immune activation, is present in the blood during inflammation, and has been found to be a target of autoantibodies and autoimmune T cells in healthy individuals and, to a greater extent, in those suffering from autoimmune diseases. Recently, HSP60 was discovered to activate macrophages by way of the innate toll-like receptor 4 (TLR4) to induce enhanced production of NO and IL-12, IL-15, TNF-α, IL-6, and other Th1-type cytokines. Thus, HSP60 would seem to be an important factor in inflammation generally. The present study was undertaken to test whether HSP60 might also exert a direct, innate effect on T cell physiology.PRINCIPAL FINDINGS1. HSP60 induces T cell adhesion to FNWe purified T cells from the peripheral blood of healthy human donors, fractioned the T cells into CD45RA+ and CD45RO+ subpopulations, incubated the T cells with var...Keywords
Funding Information
- Minerva Foundation
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