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APRIL modulates B and T cell immunity

AutorStein, Jens V.; López Fraga, Marta; Elustondo, Fernando A.; Carvalho-Pinto, Carla E.; Rodríguez Aguirre, Dolores; Gómez Caro, Ruth; Jong, Joan de; Martínez-Alonso, Carlos; Medema, Jan Paul; Hahne, Michael
Fecha de publicaciónjun-2002
EditorAmerican Society for Clinical Investigation
CitaciónThe Journal of Clinical Investigation, vol. 109(12), pp. 1587-1598, (2002)
ResumenThe 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.
DescripciónThe final version of this paper is available at: http://dx.doi.org/10.1172/JCI15034
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