11
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Heat shock protein 60 activates cytokine-associated negative regulator suppressor of cytokine signaling 3 in T cells: effects on signaling, chemotaxis, and inflammation.

      The Journal of Immunology Author Choice

      Adoptive Transfer, Animals, Cell Polarity, drug effects, Chaperonin 60, pharmacology, Chemokine CXCL12, Chemokines, CXC, Chemotaxis, Leukocyte, Cytokines, metabolism, Female, Focal Adhesion Kinase 2, Gene Silencing, Humans, In Vitro Techniques, Inflammation, etiology, immunology, Lymphocyte Activation, MAP Kinase Signaling System, Membrane Glycoproteins, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Inbred NOD, Mice, Knockout, Mice, SCID, Models, Immunological, Myosin Light Chains, Phosphorylation, Protein-Serine-Threonine Kinases, Protein-Tyrosine Kinases, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-akt, Receptors, Cell Surface, Receptors, Immunologic, Recombinant Proteins, Repressor Proteins, antagonists & inhibitors, genetics, Signal Transduction, Suppressor of Cytokine Signaling Proteins, T-Lymphocytes, physiology, Toll-Like Receptor 2, Toll-Like Receptors, Transcription Factors

      Read this article at

      ScienceOpenPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Previously, we reported that treatment of T cells with the 60-kDa heat shock protein (HSP60) inhibits chemotaxis. We now report that treatment of purified human T cells with recombinant human HSP60 or its biologically active peptide p277 up-regulates suppressor of cytokine signaling (SOCS)3 expression via TLR2 and STAT3 activation. SOCS3, in turn, inhibits the downstream effects of stromal cell-derived-1alpha (CXCL12)-CXCR4 interaction in: 1) phosphorylation of ERK1/2, Pyk2, AKT, and myosin L chain, required for cell adhesion and migration; 2) formation of rear-front T cell polarity; and 3) migration into the bone marrow of NOD/SCID mice. HSP60 also activates SOCS3 in mouse lymphocytes and inhibits their chemotaxis toward stromal cell-derived factor-1alpha and their ability to adoptively transfer delayed-type hypersensitivity. These effects of HSP60 could not be attributed to LPS or LPS-associated lipoprotein contamination. Thus, HSP60 can regulate T cell-mediated inflammation via specific signal transduction and SOCS3 activation.

          Related collections

          Author and article information

          Journal
          15972659

          Comments

          Comment on this article