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Primary lymphoid organs are pivotal in the formation, development, and maturation of lymphocytes, the white blood cells that serve as the backbone of our immune system. This crucial function underscores their fundamental role in maintaining our overall health and immunity. The two primary lymphoid organs of prime importance are the red bone marrow and the thymus.
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Related Experiment Video

Updated: Apr 26, 2026

Isolation of Precursor B-cell Subsets from Umbilical Cord Blood
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Rictor is required for early B cell development in bone marrow.

Yingchi Zhang1, Tianyuan Hu1, Chunlan Hua1

  • 1State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China; Center for Stem Cell Medicine, Chinese Academy of Medical Sciences, Beijing, China.

Plos One
|August 2, 2014
PubMed
Summary

mTORC2, regulated by Rictor, is crucial for early B cell development. Deleting Rictor impairs B cell maturation by increasing FoxO1 and Rag-1, highlighting a cell-intrinsic mechanism in hematopoiesis.

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Area of Science:

  • Immunology
  • Cell Biology
  • Hematopoiesis

Background:

  • Early B cell development from hematopoietic stem cells (HSCs) is a key model for terminal differentiation.
  • Akt signaling is vital for hematopoiesis, with mTORC2 regulating Akt.
  • The specific role of mTORC2 in early B cell development is not well understood.

Purpose of the Study:

  • To investigate the functional role of mTORC2 in early B cell development.
  • To determine the mechanism by which mTORC2 influences B cell maturation.

Main Methods:

  • Specific deletion of Rictor, an mTORC2 component, in hematopoietic cells.
  • Bone marrow (BM) transplantation assays.
  • Analysis of B cell populations in peripheral blood (PB) and spleen.
  • Assessment of FoxO1 and Rag-1 protein levels.
  • Knockdown of FoxO1 in Rictor-deleted cells.
  • Treatment with rapamycin (mTORC1 inhibitor).

Main Results:

  • Rictor deletion in BM B cells led to increased FoxO1 and Rag-1 proteins.
  • This Rictor deletion resulted in decreased B cell abundance in PB and spleen, indicating impaired early B cell development.
  • BM transplantation confirmed a cell-intrinsic defect in B cell differentiation.
  • FoxO1 knockdown in Rictor-deleted cells rescued B cell maturation.
  • Rapamycin treatment exacerbated B cell development deficiency.

Conclusions:

  • Rictor-dependent mTORC2 signaling is essential for normal early B cell development.
  • Rictor regulates B cell maturation in a cell-intrinsic manner.
  • The mechanism involves the modulation of FoxO1 and Rag-1 expression by Rictor.