Active immunization against gonadotropin-releasing hormone enhances the generation of B cells but does not affect their colonization in peripheral immune organs in male rats.

Abstract

Active immunization against gonadotropin-releasing hormone (GnRH) affects the immune system by inhibiting testosterone production. Our previous study investigated the effects of GnRH immunization on thymic T-cell generation, migration, and colonization in peripheral immune organs. However, the mechanisms by which GnRH immunization influences B cell generation and the characteristics of B cell colonization in peripheral immune organs remain unclear. Herein, GnRH immunization enhanced B cell generation by reducing apoptosis. GnRH immunization did not markedly affect the cell cycle of bone marrow cells, B cell development-related signaling molecules, or the percentage of B cells in the blood, spleen, or inguinal lymph nodes. After testosterone supplementation in GnRH-immunocastrated rats, the generation of B cells in the bone marrow was significantly reduced, and the apoptosis of B cells was remarkably increased. Testosterone did not significantly affect the cell cycle of bone marrow cells or the proportion of B cells in the blood, spleen, or inguinal lymph nodes of the GnRH-immunocastrated rats. Overall, these results clarify the mechanisms related to B cell expansion in the bone marrow and the settlement characteristics of B cells in peripheral immune organs after GnRH immunization.