| First Author | Taguchi N | Year | 2001 |
| Journal | J Autoimmun | Volume | 16 |
| Issue | 4 | Pages | 393-400 |
| PubMed ID | 11437487 | Mgi Jnum | J:70163 |
| Mgi Id | MGI:2136523 | Doi | 10.1006/jaut.2001.0515 |
| Citation | Taguchi N, et al. (2001) B Cells are Selectively Associated with Thymic Cortical but not Medullary Pathology in NZB Mice. J Autoimmun 16(4):393-400 |
| abstractText | Abnormal expansion of autoantibody-synthesizing B cells and self-reactive T cells, which most likely escape negative selection within the thymus, have both been characterized and reasoned to play a role in the pathogenesis of autoimmunity in NZB mice. Support for this thesis has been our observation that NZB mice have severe cortical and medullary thymic microarchitectural defects. As a means to dissect the roles of T and B cells in the induction of such abnormalities, B cell-deficient NZB mice were bred by backcrossing the Igh6(null)allele on to the NZB background (NZB-&mgr;MT mice). Such mice showed undetectable levels of autoantibodies. NZB-&mgr;MT mice, as compared to wild-type NZB mice, had lower absolute numbers of CD4(+)T cells. Furthermore, thymic abnormalities in NZB-&mgr;MT mice were restricted to the medulla. These data suggest that, while B cells may play a role in thymic cortical abnormalities, the medullary abnormalities are induced by other mechanisms. Copyright 2001 Academic Press. |
