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© Charles Dauguet
Virus VIH-1 (HIV-1), agent du sida, à la surface d'un lymphocyte. Image colorisée.
Publication : Oncoimmunology

TCR-dependent sensitization of human γδ T cells to non-myeloid IL-18 in cytomegalovirus and tumor stress surveillance

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Oncoimmunology - 01 May 2015

Guerville F, Daburon S, Marlin R, Lartigue L, Loizon S, Pitard V, Couzi L, Moreau JF, Déchanet-Merville J, Faustin B

Link to Pubmed [PMID] – 26155394

Oncoimmunology 2015 May;4(5):e1003011

Human γδ T cells contribute to tissue homeostasis under normal conditions and participate in lymphoid stress surveillance against infection and tumors. However, the molecular mechanisms underlying the recognition of complex cell stress signatures by γδ T cells are still unclear. Tumor cells and human cytomegalovirus (HCMV)-infected cells are known targets of γδ T cells. We show here that many tumor and CMV-infected cells express caspase-1 inflammasomes and release interleukin (IL)-18. Engagement of the T-cell receptor (TCR) on Vδ2(neg) γδ T cells controlled the direct innate immune sensing of IL-18 that enhanced cytotoxicity and interferon gamma (IFNγ) production. This TCR-dependent sensitization to IL-18 was mediated by the upregulation of the innate IL-18 receptor β chain (IL-18Rβ) expression. These findings shed light on inflammasomes as a unified stress signal of tumor and infected cells to alert γδ T cells. Moreover, uncovering the TCR-mediated sensitization of γδ T cells to inflammatory mediators establishes a molecular link between the innate and adaptive immune functions of γδ T cells that could fine tune the commitment of antigen-experienced γδ T cells to inflammatory responses.

http://www.ncbi.nlm.nih.gov/pubmed/26155394