| First Author | Ikarashi Y | Year | 2001 |
| Journal | J Exp Med | Volume | 194 |
| Issue | 8 | Pages | 1179-86 |
| PubMed ID | 11602646 | Mgi Jnum | J:72170 |
| Mgi Id | MGI:2151958 | Doi | 10.1084/jem.194.8.1179 |
| Citation | Ikarashi Y, et al. (2001) Dendritic Cell Maturation Overrules H-2D-mediated Natural Killer T (NKT) Cell Inhibition. Critical role for b7 in cd1d-dependent nkt cell interferon gamma production. J Exp Med 194(8):1179-86 |
| abstractText | 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. |
