Calcineurin/NFAT signaling and innate host defence: a role for NOD1-mediated phagocytic functions

Cell Communication and Signaling

Review

Alain Vandewalle¹  Emilie Tourneur¹  Marcelle Bens¹  Cécilia Chassin¹  Catherine Werts² 

[1] Centre de Recherche sur l’Inflammation (CRI), UMRS 1149 et Groupe ATIP-AVENIR, Université Denis Diderot – Paris 7, Paris, France;Institut Pasteur, Unité Biologie et génétique des parois bactériennes, Paris, France;

关键词: NFAT;    Calcineurin inhibitors;    NOD1;    Bacterial phagocytosis;   

DOI  :  10.1186/1478-811X-12-8

 received in 2013-12-02, accepted in 2014-01-23,  发布年份 2014

来源: Springer

【 摘 要 】

The calcineurin/nuclear factor of activated T cells (NFATs) signaling pathway plays a central role in T cell mediated adaptive immune responses, but a number of recent studies demonstrated that calcineurin/NFAT signaling also plays a key role in the control of the innate immune response by myeloid cells. Calcineurin inhibitors, such as cyclosporine A (CsA) and tacrolimus (FK506), are commonly used in organ transplantation to prevent graft rejection and in a variety of immune diseases. These immunosuppressive drugs have adverse effects and significantly increase host’s susceptibility towards bacterial or fungal infections. Recent studies highlighted the role of NFAT signaling in fungal infection and in the control of the pattern recognition receptor nucleotide-binding oligomerization domain-containing protein 1 (NOD1), which predominantly senses invasive Gram-negative bacteria and mediates neutrophil phagocytic functions. This review summarises some of the current knowledge concerning the role of NFAT signaling in the innate immune response and the recent advances on NFAT-dependent inhibition of NOD1-mediated innate immune response caused by CsA, which may contribute to sensitizing transplant recipients to bacterial infection.

【 授权许可】

CC BY   
© Vandewalle et al.; licensee BioMed Central Ltd. 2014