Soluble MICA-NKG2D interaction upregulates IFN-γ production by activated CD3-CD56+ NK cells: Potential impact on chronic graft versus host disease

Wahid Boukouaci, Reem Al-Daccak, Nicolas Dulphy, Laura Lauden, Kahina Amokrane, Catherine Fortier, François Marzais, Meriem Bennabi, Regis Peffault de Latour, Gerard Socie, Antoine Toubert, Dominique Charron, Rajagopal Krishnamoorthy, Ryad Tamouza

Résultats de recherche: Contribution à un journalArticleRevue par des pairs

10 Citations (Scopus)

Résumé

A soluble isoform of MHC class I chain-related molecule A (soluble MICA), generated by proteolytic shedding from the membrane-bound MICA of various tumor cells, has been shown to downregulate both the expression of natural killer group 2-member D receptor and the cytotoxic function of effectors cells and was postulated as a mechanism for tumor immune evasion. Its effect on the expression of cytokines by the effector cells remained unexplored. Here we demonstrate that the sMICA molecules upregulate interferon gamma expression by interleukin-12/interleukin-18-activated CD3-CD56+ natural killer cells, witnessing the pro-inflammatory effect of soluble MICA. Overall, these data are in line with our previous observations that the raised serum levels of soluble MICA, following allogeneic hematopoietic stem cell transplantation, confer susceptibility to and the presence of pre-transplantation anti-MICA antibodies in the patient's serum confer protection against chronic graft versus host disease.

langue originaleAnglais
Pages (de - à)1536-1541
Nombre de pages6
journalHuman Immunology
Volume74
Numéro de publication12
Les DOIs
étatPublié - 4 oct. 2013
Modification externeOui

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