Cutting Edge: CD4 Is the Receptor for the Tick Saliva Immunosuppressor, Salp15

  • Renu Garg
    Department of Biology, University of North Carolina at Charlotte , Charlotte, NC 28223
  • Ignacio J Juncadella
    Department of Biology, University of North Carolina at Charlotte , Charlotte, NC 28223
  • Nandhini Ramamoorthi
    Department of Internal Medicine, Section of Rheumatology, Yale University School of Medicine , New Haven, CT 06520
  • Ashish
    Department of Chemistry, University of North Carolina at Charlotte , Charlotte, NC 28223
  • Shobana K Ananthanarayanan
    Department of Biology, University of North Carolina at Charlotte , Charlotte, NC 28223
  • Venetta Thomas
    Department of Internal Medicine, Section of Rheumatology, Yale University School of Medicine , New Haven, CT 06520
  • Mercedes Rincón
    Department of Internal Medicine, Section of Immunobiology, University of Vermont , Burlington, VT 05405
  • Joanna K Krueger
    Department of Chemistry, University of North Carolina at Charlotte , Charlotte, NC 28223
  • Erol Fikrig
    Department of Internal Medicine, Section of Rheumatology, Yale University School of Medicine , New Haven, CT 06520
  • Christopher M Yengo
    Department of Biology, University of North Carolina at Charlotte , Charlotte, NC 28223
  • Juan Anguita
    Department of Biology, University of North Carolina at Charlotte , Charlotte, NC 28223

書誌事項

公開日
2006-11
権利情報
  • https://academic.oup.com/pages/standard-publication-reuse-rights
DOI
  • 10.4049/jimmunol.177.10.6579
公開者
Oxford University Press (OUP)

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説明

<jats:title>Abstract</jats:title> <jats:p>Salp15 is an Ixodes scapularis salivary protein that inhibits CD4+ T cell activation through the repression of TCR ligation-triggered calcium fluxes and IL-2 production. We show in this study that Salp15 binds specifically to the CD4 coreceptor on mammalian host T cells. Salp15 specifically associates through its C-terminal residues with the outermost two extracellular domains of CD4. Upon binding to CD4, Salp15 inhibits the subsequent TCR ligation-induced T cell signaling at the earliest steps including tyrosine phosphorylation of the Src kinase Lck, downstream effector proteins, and lipid raft reorganization. These results provide a molecular basis to understanding the immunosuppressive activity of Salp15 and its specificity for CD4+ T cells.</jats:p>

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