| First Author | Gunn MD | Year | 1999 |
| Journal | J Exp Med | Volume | 189 |
| Issue | 3 | Pages | 451-60 |
| PubMed ID | 9927507 | Mgi Jnum | J:52567 |
| Mgi Id | MGI:1329766 | Doi | 10.1084/jem.189.3.451 |
| Citation | Gunn MD, et al. (1999) Mice lacking expression of secondary lymphoid organ chemokine have defects in lymphocyte homing and dendritic cell localization [see comments]. J Exp Med 189(3):451-60 |
| abstractText | Secondary lymphoid organ chemokine (SLC) is expressed in high endothelial venules and in T cell zones of spleen and lymph nodes (LNs) and strongly attracts naive T cells. In mice homozygous for the paucity of lymph node T cell (plt) mutation, naive T cells fail to home to LNs or the lymphoid regions of spleen. Here we demonstrate that expression of SLC is undetectable in pit mice. In addition to the defect in T cell homing, we demonstrate that dendritic cells (DCs) fail to accumulate in spleen and LN T cell zones of plt mice. DC migration to LNs after contact sensitization is also substantially reduced. The physiologic significance of these abnormalities in pit mice is indicated by a markedly increased sensitivity to infection with murine hepatitis virus. The pit mutation maps to the :SLC locus; however, the sequence of SLC introns and exons in plt mice is normal. These findings suggest that the abnormalities in pit mice are due to a genetic defect in the expression of SLC and that SLC mediates the entry of naive T cells and antigen-stimulated DCs into the T cell zones of secondary lymphoid organs. |
