| First Author | Campos RA | Year | 2003 |
| Journal | J Exp Med | Volume | 198 |
| Issue | 12 | Pages | 1785-96 |
| PubMed ID | 14676294 | Mgi Jnum | J:132827 |
| Mgi Id | MGI:3777025 | Doi | 10.1084/jem.20021562 |
| Citation | Campos RA, et al. (2003) Cutaneous immunization rapidly activates liver invariant Valpha14 NKT cells stimulating B-1 B cells to initiate T cell recruitment for elicitation of contact sensitivity. J Exp Med 198(12):1785-96 |
| abstractText | T cell recruitment to elicit contact sensitivity (CS) requires a CS-initiating process mediated by B-1 cells that produce IgM, which activates complement to promote T cell passage into the tissues. We now show that Valpha14i NKT cells induce B-1 cell activation likely by releasing IL-4 early postimmunization. The CS initiation process is absent in Jalpha18-/- and CD1d-/- NKT cell-deficient mice and is reconstituted by populations enriched for Valpha14i NKT cells. Transfers are not effective if cells are derived from IL-4-/- mice. Staining with specific tetramers directly showed that hepatic Valpha14i NKT cells increase by 30 min and nearly double by 2 h postimmunization. Transfer of immune B-1 cells also reconstitutes CS responses in NKT cell-deficient mice. The B-1 cells act downstream of the Valpha14i NKT cells to restore CS initiation. In addition, IL-4 given systemically to Jalpha18-/- or CD1d-/- NKT cell-deficient mice reconstitutes elicitation of CS. Further, splenocytes from immune Jalpha18-/- mice produce less antigen (Ag)-specific IgM antibodies compared with sensitized WT mice. Together these findings indicate that very early after skin immunization Valpha14i NKT cells are stimulated to produce IL-4, which activates B-1 cells to produce Ag-specific IgM, subsequently needed to recruit effector T cells for elicitation of CS responses. |
