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Brief Definitive Report

: Critical Role for B7 in Cd1d-Dependent Nkt Cell Interferon Production

Yoshinori Ikarashi^a, Rumiko Mikami^a, Albert Bendelac^b, Magali Terme^a, Nathalie Chaput^a, Masahiro Terada^d, Thomas Tursz^a, Eric Angevin^a, François A. Lemonnier^c, Hiro Wakasugi^d, and Laurence Zitvogel^a

^a Unité d'Immunologie, Département de Biologie Clinique, Institut Gustave Roussy, 94805 Villejuif Cedex, France
^b Princeton University, Princeton, NJ 08544
^c Unité d'Immunologie Cellulaire Antivirale, Institut Pasteur, Paris 75015, France
^d Pharmacology Division, National Cancer Center, Tokyo 104-0045, Japan
Unité d'Immunologie, Département de Biologie Clinique, (+12) Institut Gustave Roussy 39, rue Camille Desmoulins, 94805 Villejuif, France.33-1-42-11-60-9433-1-42-11-50-41

zitvogel{at}igr.fr

Given the broad expression of H-2 class Ib molecules on hematopoietic cells, antigen presentation pathways among CD1d expressing cells might tightly regulate CD1d-restricted natural killer T (NKT) cells. Bone marrow–derived dendritic cells (BM-DCs) and not adherent splenocytes become capable of triggering NK1.1⁺/T cell receptor (TCR)^int hepatic NKT cell activation when (a) immature BM-DCs lack H-2D^b–^/– molecules or (b) BM-DCs undergo a stress signal of activation. In such conditions, BM-DCs promote T helper type 1 predominant CD1d-restricted NKT cell stimulation. H-2 class Ia–mediated inhibition involves more the direct H-2D^b presentation than the indirect Qa-1^b pathway. Such inhibition can be overruled by B7/CD28 interactions and marginally by CD40/CD40L or interleukin 12. These data point to a unique regulatory role of DCs in NKT cell innate immune responses and suggest that H-2 class Ia and Ib pathways differentially control NKT cell recognition of DC antigens.

Key Words: inhibitory receptors • IFN- • costimulation • CD1d • NKT cells

© 2001 The Rockefeller University Press

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