| First Author | Imada M | Year | 2009 |
| Journal | Int Immunol | Volume | 21 |
| Issue | 10 | Pages | 1151-61 |
| PubMed ID | 19684158 | Mgi Jnum | J:153772 |
| Mgi Id | MGI:4366215 | Doi | 10.1093/intimm/dxp081 |
| Citation | Imada M, et al. (2009) Ectopically expressed PIR-B on T cells constitutively binds to MHC class I and attenuates T helper type 1 responses. Int Immunol 21(10):1151-61 |
| abstractText | Activated mature T cells induce various inhibitory receptors implicated in maintaining peripheral tolerance in response to the trans-acting ligands. Interestingly, paired Ig-like receptor (PIR)-B, an inhibitory MHC class I receptor on B cells and myeloid cells, could be involved in regulating early T cell development because epitope for PIR is detected on pre-thymic T/NK progenitors but not on thymocytes or mature T cells. We hypothesized that PIR-B is not only a regulator for T cell development but is also detrimental if expressed on mature T cells. Here we demonstrated, using PIR-B-deficient fetuses, that PIR-B is indeed expressed on the T cell progenitors but failed to identify its distinctive roles in the development. Forced expression of PIR-B in thymocytes and mature T cells also resulted in no abnormalities in development. However, upon antigenic or allogeneic stimulation, peripheral T cells with the ectopic PIR-B showed reduced T(h) type 1 responses due to the suppression of proximal TCR signaling by constitutive binding of PIR-B to MHC class I on the same cell surface. Our findings suggest that T cell expression of PIR-B with the cis-interacting MHC class I is strictly prohibited in periphery so as to secure prompt immune responses. |
