| First Author | Bommireddy R | Year | 2004 |
| Journal | Cell Immunol | Volume | 232 |
| Issue | 1-2 | Pages | 96-104 |
| PubMed ID | 15922720 | Mgi Jnum | J:99033 |
| Mgi Id | MGI:3580986 | Doi | 10.1016/j.cellimm.2005.02.004 |
| Citation | Bommireddy R, et al. (2004) Elimination of both CD4(+) and CD8(+) T cells but not B cells eliminates inflammation and prolongs the survival of TGFbeta1-deficient mice. Cell Immunol 232(1-2):96-104 |
| abstractText | Transforming growth factor beta1 (TGFbeta1) is a potent negative immunoregulatory molecule. We have previously shown that the autoimmune-mediated weaning-age lethality of Tgfb1(-/-) mice is reversed upon genetic combination with Scid or Rag null alleles. Here, we show that elimination of T but not B cells is sufficient for the reversal, but elimination of either CD4(+) or CD8(+) cells is not. Although elimination of B cells does not rescue TGFbeta1-deficient animals from autoimmunity, B cells are hyperresponsive to LPS in the absence of TGFbeta1. TGFbeta1 deficiency leads to activation of CD8(+) T cells as suggested by down-modulation of CD8 even in the absence of CD4(+) T cells. This study provides evidence that both CD4(+) and CD8(+) T cells, but not B cells, have the ability to cause inflammation in the absence of TGFbeta1. However, though TGFbeta1-deficient B cells are hyperresponsive to stimulation, alone they are not sufficient to cause inflammation. |
