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Dendritic Cell Maturation Overrules H-2D–mediated Natural Killer T (NKT) Cell Inhibition: Critical Role for B7 in CD1d-dependent NKT Cell Interferon Production

Correspondence to: Laurence Zitvogel, Unité d'Immunologie, Département de Biologie Clinique, (+12) Institut Gustave Roussy 39, rue Camille Desmoulins, 94805 Villejuif, France. Tel:33-1-42-11-50-41 Fax:33-1-42-11-60-94 E-mail: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

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