Review Article | Published:

Insights into the initiation of TCR signaling

Nature Immunology volume 15, pages 798807 (2014) | Download Citation

Abstract

The initiation of T cell antigen receptor signaling is a key step that can result in T cell activation and the orchestration of an adaptive immune response. Early events in T cell receptor signaling can distinguish between agonist and endogenous ligands with exquisite selectivity, and show extraordinary sensitivity to minute numbers of agonists in a sea of endogenous ligands. We review our current knowledge of models and crucial molecules that aim to provide a mechanistic explanation for these observations. Building on current understanding and a discussion of unresolved issues, we propose a molecular model for initiation of T cell receptor signaling that may serve as a useful guide for future studies.

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Acknowledgements

We thank M. Fruschicheva for help with the references. We also thank K. Vicari of the Nature Publishing Group for her artistic work on the figures in this article. This work was supported, in part, by a grant from the US National Institutes of Health (PO1 AI091580 to A.K.C. and A.W.).

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Affiliations

  1. Department of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA.

    • Arup K Chakraborty
  2. Department of Physics, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA.

    • Arup K Chakraborty
  3. Department of Chemistry, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA.

    • Arup K Chakraborty
  4. Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA.

    • Arup K Chakraborty
  5. Institute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA.

    • Arup K Chakraborty
  6. Ragon Institute of MGH, MIT and Harvard, Cambridge, Massachusetts, USA.

    • Arup K Chakraborty
  7. Rosalind Russell/Ephraim P. Engleman Rheumatology Research Center, Division of Rheumatology, Department of Medicine and the Howard Hughes Medical Institute, University of California at San Francisco, San Francisco, California, USA.

    • Arthur Weiss

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The authors declare no competing financial interests.

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Correspondence to Arthur Weiss.

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https://doi.org/10.1038/ni.2940

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