| First Author | Stein JV | Year | 2002 |
| Journal | J Clin Invest | Volume | 109 |
| Issue | 12 | Pages | 1587-98 |
| PubMed ID | 12070306 | Mgi Jnum | J:77325 |
| Mgi Id | MGI:2181358 | Doi | 10.1172/JCI15034 |
| Citation | Stein JV, et al. (2002) APRIL modulates B and T cell immunity. J Clin Invest 109(12):1587-98 |
| abstractText | The TNF-like ligands APRIL and BLyS are close relatives and share the capacity to bind the receptors TACI and BCMA. BLyS has been shown to play an important role in B cell homeostasis and autoimmunity, but the biological role of APRIL remains less well defined. Analysis of T cells revealed an activation-dependent increase in APRIL mRNA expression. We therefore generated mice expressing APRIL as a transgene in T cells. These mice appeared normal and showed no signs of B cell hyperplasia. Transgenic T cells revealed a greatly enhanced survival in vitro as well as enhanced survival of staphylococcal enterotoxin B-reactive CD4+ T cells in vivo, which both directly correlate with elevated Bcl-2 levels. Analysis of humoral responses to T cell-dependent antigens in the transgenic mice indicated that APRIL affects only IgM but not IgG responses. In contrast, T cell-independent type 2 (TI-2) humoral response was enhanced in APRIL transgenic mice. As TACI was previously reported to be indispensable for TI-2 antibody formation, these results suggest a role for APRIL/TACI interactions in the generation of this response. Taken together, our data indicate that APRIL is involved in the induction and/or maintenance of T and B cell responses. |
