Annual Review of Immunology Volume 28 2010 by Annual Reviews

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CYTOSOL D V A N ANRV406-IY28-02 ARI 18 August 2009 17:39 a Periphery Bone marrow Antigen-independent Antigen-dependent Antigen-dependent Igμ Igα/Igβ Prepro-B Stem cell Pro-B Igμ φL Large pre-B mIgM mIgD mIgM Igκ or Igλ Small pre-B Immature B Transitional B Mature B Annu. Rev. Immunol. 28. org by UNIVERSITY OF IOWA on 01/28/10. For personal use only. Autoreactive Dμ Receptor editing Deletion or anergy RAG: - Low + - + Low - - IgH: GL GL DJH VHDJH - - - - IgL: GL GL GL GL VLJL VLJL? 16 C E I N A D V A N Kurosaki · Shinohara · Baba IL-7 ARI 18 August 2009 17:39 regulated at the level of VH gene accessibility and appears to require the cytokine IL-7, the transcription factors Pax5 and YY1, and high levels of Rag1/Rag2 (13, 140–143).

In contrast to Act1’s involvement in both CD40 and BAFFR signaling, BANK plays a negative role only in CD40 signaling, presumably through the inhibition of CD40-mediated Akt activation (217). In B cells, Bcl6 is a master regulator of GC commitment, maintenance, and suppression of PC differentiation (212, 218). Thus, it is important to clarify when and how Bcl6 is turned on and off. However, these questions have not yet been adequately addressed. With regard to the mechanisms by which Bcl6 is turned off, signaling through the BCR and CD40 has been implicated.

Unlike other TRAFs (such as TRAF2, TRAF5, and TRAF6), TRAF3 does not activate the canonical NFκB or JNK pathway (191). Instead, TRAF3, in the resting state, suppresses the noncanonical NF-κB pathway by binding NIK and targeting it for proteosomal degradation (192). NIK is responsible for directly phosphorylating and activating IKKα and the subsequent activation of the noncanonical pathway (193, 194). Activated BAFFR recruits TRAF3, allowing B cells to terminate TRAF3-mediated degradation of NIK.

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