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

Journal Article (Journal Article)

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.

Full Text

Duke Authors

Cited Authors

  • Ci, X; Kuraoka, M; Wang, H; Carico, Z; Hopper, K; Shin, J; Deng, X; Qiu, Y; Unniraman, S; Kelsoe, G; Zhong, X-P

Published Date

  • 2015

Published In

Volume / Issue

  • 10 / 5

Start / End Page

  • e0127527 -

PubMed ID

  • 26000908

Pubmed Central ID

  • PMC4441391

Electronic International Standard Serial Number (EISSN)

  • 1932-6203

Digital Object Identifier (DOI)

  • 10.1371/journal.pone.0127527


  • eng

Conference Location

  • United States