| First Author | Klonowski KD | Year | 2006 |
| Journal | J Immunol | Volume | 177 |
| Issue | 10 | Pages | 6738-46 |
| PubMed ID | 17082587 | Mgi Jnum | J:140494 |
| Mgi Id | MGI:3813995 | Doi | 10.4049/jimmunol.177.10.6738 |
| Citation | Klonowski KD, et al. (2006) CD8 T cell recall responses are regulated by the tissue tropism of the memory cell and pathogen. J Immunol 177(10):6738-46 |
| abstractText | Whether memory CD8 T cells can be reactivated in nonlymphoid tissues is unclear. Using mice lacking the spleen, lymph nodes, or both, we show that the secondary T cell response, but not homeostatic maintenance of memory cells, required lymphoid tissue. Whereas primary and secondary CD8 T cell responses to vesicular stomatitis virus infection were lymph node dependent, responses to Listeria monocytogenes infection were driven primarily in the spleen. Memory cell subset reactivation was also regulated by location of the responding population and the pathogen. Thus, CD62Llow effector memory T cells (TEM) cells responded nearly as well as CD62Lhigh central memory T cells (TCM) and TCM cells after L. monocytogenes infection, and both subsets generated equivalent populations of secondary memory cells. In contrast, TCM cells, but not TEM cells, mounted a robust response to vesicular stomatitis virus infection. TCM and TEM cells also required lymphoid tissue to mount recall responses, and the bone marrow did not contribute significantly to the response of either subset. Our findings indicated that characteristics of the infectious agent and the migratory preferences of memory cells dictated the secondary lymphoid tissue requirement for the recall response to infection. |
