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PD-1 induction through TCR activation is partially regulated by endogenous TGF-β

Cellular & Molecular Immunology volume 12, pages 648–649 (2015)Cite this article

The programmed death 1 (PD-1) pathway is a way of inhibiting T-cell proliferation and cytokine production. This pathway is important for maintaining peripheral tolerance. Different mechanisms and cytokines are involved in this pathway. Herein, we show the contribution of endogenous TGF-β to increasing PD-1 expression after T cell receptor (TCR) activation.

The receptor for PD-1, also called CD279, is a regulatory protein of the CD28 family and is expressed at low levels on the surface of resting T and B lymphocytes.1 PD-1 is induced by the expression of TCR or B-cell receptor signaling.2 Its induction on the surface of activated T cells can prevent a runaway immune response. Indeed, the interaction between PD-1 and its ligand (PD-L1 or PD-L2) inhibits proliferation and effector functions of T cells and induces apoptosis.1,3 The regulatory pathway PD-1 thus constitutes a safeguard against autoimmunity and excessive tissue destruction by T cells.3 Conversely, it can be involved in tumor escape if it is hyperactivated in tumor-infiltrating CD8+T cells.4

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Authors and Affiliations

  1. Laboratory of Transmission, Control and Immunobiology of Infection, Institut Pasteur de Tunis, Tunis, Tunisia

    Raja Rekik, Nadia Belhadj Hmida & Melika Ben Ahmed

  2. Laboratory of Clinical Immunology, Institut Pasteur de Tunis, Tunis, Tunisia

    Ahlem Ben Hmid, Imen Zamali, ns Kammoun & Melika Ben Ahmed

  3. Faculté de Médecine de Tunis, Université Tunis El Manar, Tunis, Tunisia

    Ahlem Ben Hmid & Melika Ben Ahmed

Authors
  1. Raja Rekik
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  2. Nadia Belhadj Hmida
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  3. Ahlem Ben Hmid
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  4. Imen Zamali
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  5. ns Kammoun
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  6. Melika Ben Ahmed
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Correspondence to Melika Ben Ahmed.

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Rekik, R., Belhadj Hmida, N., Ben Hmid, A. et al. PD-1 induction through TCR activation is partially regulated by endogenous TGF-β. Cell Mol Immunol 12, 648–649 (2015). https://doi.org/10.1038/cmi.2014.104

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  • DOI: https://doi.org/10.1038/cmi.2014.104

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