TSC1 Promotes B Cell Maturation but Is Dispensable for Germinal Center Formation.

Abstract

Accumulating evidence indicates that the tuberous sclerosis complex 1 (TSC1), a tumor suppressor that acts by inhibiting mTOR signaling, plays an important role in the immune system. We report here that TSC1 differentially regulates mTOR complex 1 (mTORC1) and mTORC2/Akt signaling in B cells. TSC1 deficiency results in the accumulation of transitional-1 (T1) B cells and progressive losses of B cells as they mature beyond the T1 stage. Moreover, TSC1KO mice exhibit a mild defect in the serum antibody responses or rate of Ig class-switch recombination after immunization with a T-cell-dependent antigen. In contrast to a previous report, we demonstrate that both constitutive Peyer's patch germinal centers (GCs) and immunization-induced splenic GCs are unimpaired in TSC1-deficient (TSC1KO) mice and that the ratio of GC B cells to total B cells is comparable in WT and TSC1KO mice. Together, our data demonstrate that TSC1 plays important roles for B cell development, but it is dispensable for GC formation and serum antibody responses.

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10.1371/journal.pone.0127527

Publication Info

Ci, Xinxin, Masayuki Kuraoka, Hongxia Wang, Zachary Carico, Kristen Hopper, Jinwook Shin, Xuming Deng, Yirong Qiu, et al. (2015). TSC1 Promotes B Cell Maturation but Is Dispensable for Germinal Center Formation. PLoS One, 10(5). p. e0127527. 10.1371/journal.pone.0127527 Retrieved from https://hdl.handle.net/10161/10894.

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