摘要
Interleukin （IL）-15 is known to strongly modulate T-cell function; however, its role in controlling mucosal immunity, including its ability to modulate B-la cell activity, remains to be elucidated. Here, we show that IL-15 upregulates activation molecules and the costimulatory molecule CD80 on viable B-la cells. Cell activation was accompanied by the depletion of sialic acid-binding immunoglobulin-like lectin （Siglec）-G, an inhibitor of cell activation that is present on B-la cells. The IL-15 receptor CD122 was stimulated on B-la cells by the cytokine showing its direct involvement in IL-15-mediated responses. IL-IO is responsible for the long term survival of B-la cells in culture, which is initially promoted by IL-15. The upregulation of IL-IO was followed by the appearance of suppressor of cytokine signaling （SOCS）I in the presence of IL-15 and the loss of IL-IO. This resulted in the cells switching to IL-12 expression. This anti-inflammatory to pro-inflammatory shift in the B-la cell character was independent of the cell-specific marker CD5, which remained highly expressed throughout the in vitro life of the cells. The presence of the immunosuppressive receptor programmed cell death （PD）-I and its ligand PD-L2 were features of a predominantly IL-IO response. PD-1 and PD-L2 can mediate juxtacrine signaling. However, the abrogation of PD-1 and its ligand was observed when the cells expressed IL-12. This demonstrates an inverse relationship between the receptor and ligand and the pro-inflammatory cytokine. The induction of IgM and IgA, which can play pivotal roles in mucosal immunity, was promoted in the presence of IL-15. Collectively, the data implicate IL-15 as the master cytokine that induces B-la cells to mount a mucosal immune response.
Interleukin （IL）-15 is known to strongly modulate T-cell function; however, its role in controlling mucosal immunity, including its ability to modulate B-la cell activity, remains to be elucidated. Here, we show that IL-15 upregulates activation molecules and the costimulatory molecule CD80 on viable B-la cells. Cell activation was accompanied by the depletion of sialic acid-binding immunoglobulin-like lectin （Siglec）-G, an inhibitor of cell activation that is present on B-la cells. The IL-15 receptor CD122 was stimulated on B-la cells by the cytokine showing its direct involvement in IL-15-mediated responses. IL-IO is responsible for the long term survival of B-la cells in culture, which is initially promoted by IL-15. The upregulation of IL-IO was followed by the appearance of suppressor of cytokine signaling （SOCS）I in the presence of IL-15 and the loss of IL-IO. This resulted in the cells switching to IL-12 expression. This anti-inflammatory to pro-inflammatory shift in the B-la cell character was independent of the cell-specific marker CD5, which remained highly expressed throughout the in vitro life of the cells. The presence of the immunosuppressive receptor programmed cell death （PD）-I and its ligand PD-L2 were features of a predominantly IL-IO response. PD-1 and PD-L2 can mediate juxtacrine signaling. However, the abrogation of PD-1 and its ligand was observed when the cells expressed IL-12. This demonstrates an inverse relationship between the receptor and ligand and the pro-inflammatory cytokine. The induction of IgM and IgA, which can play pivotal roles in mucosal immunity, was promoted in the presence of IL-15. Collectively, the data implicate IL-15 as the master cytokine that induces B-la cells to mount a mucosal immune response.
