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Gene Review

Tnfrsf13c  -  tumor necrosis factor receptor superfamily...

Mus musculus

Synonyms: 2010006P15Rik, B-cell maturation defect, B-cell-activating factor receptor, BAFF receptor, BAFF-R, ...
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Disease relevance of Tnfrsf13c

  • Unexpectedly, the BAFF-R mutation in MRL-lpr mice did not result in decreased autoantibody production, hypergammaglobulinaemia or immune complex-mediated glomerulonephritis [1].
  • Further studies found increased numbers of B cells in the bone marrow of BAFF-R-mutant MRL-lpr mice compared to the BAFF-R-intact lupus mice [1].
  • By replacing BAFF-R signals, constitutive canonical NF-kappaB signaling, a hallmark of various B cell lymphomas, causes accumulation of resting B cells and promotes their proliferation and survival upon activation, but does not per se induce lymphomagenesis [2].
  • Recent studies on BAFF, a member of the tumor necrosis factor family, and the discovery of a new BAFF receptor have revealed that this ligand-receptor pair is essential for B-cell survival and differentiation, holding promise for a better understanding and treatment of some autoimmune diseases and lymphomas [3].
  • Several QTLs controlled the mastocytosis in this intercross, and it was not possible to determine whether any of them co-segregated with Bcmd-1 [4].

High impact information on Tnfrsf13c

  • In a Perspective, Waldschmidt and Noelle discuss new findings showing that the TNF family ligand BAFF and its receptor BAFF-R are crucial for selecting transitional B cells into the mature B cell pool (Thompson et al., Schiemann et al.) [5].
  • In addition, canonical NF-kappaB activity mediates differentiation and proper localization of follicular and marginal zone B cells in the absence of BAFF-R, but not CD19 [2].
  • TNF receptor (TNFR) superfamily members, CD40, and BAFFR play critical roles in B cell survival and differentiation [6].
  • These findings demonstrate that Act1 plays an important role in the homeostasis of B cells by attenuating CD40 and BAFFR signaling [6].
  • Heightened expression of B cell maturation antigen (BCMA), and lowered expression of transmembrane activator and cyclophilin ligand interactor and BAFF receptor in PCs relative to resting B cells suggests a vital role of BCMA in PC survival [7].

Biological context of Tnfrsf13c


Anatomical context of Tnfrsf13c


Associations of Tnfrsf13c with chemical compounds

  • The Br3 antibody, which specifically recognizes CldUrd, was applied first, followed by indirect staining with goat anti-mouse phycoerythrin [14].

Regulatory relationships of Tnfrsf13c

  • These studies clearly demonstrate that BAFF regulates Ab responses in vivo through receptors in addition to BAFF-R [15].
  • In addition, we propose that BAFF-R signaling enhances the expression of survival genes through direct chromatin modifications in NF-kappa B target gene promoters [16].

Other interactions of Tnfrsf13c

  • A BAFF-specific receptor (BAFF-R; BR3) appears to mediate these functions via activation of the NF-kappaB2 pathway [8].
  • Therefore, our data suggest that the BAFF-R-mediated survival signal, provided by PLC-gamma2, is not sufficient to promote B cell maturation, and that, in addition, activation of PLC-gamma2 by BCR is required for B cell development [11].
  • This indicates that BASH-mediated BCR signaling primarily controls B cell survival and maturation, with BAFF-R signaling and its inhibition of PKCdelta acting as a secondary regulator [17].
  • In addition, Bcmd-2 or a linked locus controls mastocytosis, while Bcmd-1 does not, as indicated by splenic mast cell analysis in the congenic strains [4].
  • We have used the CBA/N X-linked B-cell maturation defect (xid) as a probe to analyse the B-cell subset involved in spontaneous anti-DNA production in MRL/1 and NZB mice [18].

Analytical, diagnostic and therapeutic context of Tnfrsf13c

  • Three polyclonal antisera recognizing the uncleaved native toxin could be found using an ELISA test (Br3, Bro2, Bro5) [19].


  1. Unexpected development of autoimmunity in BAFF-R-mutant MRL-lpr mice. Ju, Z.L., Shi, G.Y., Zuo, J.X., Zhang, J.W. Immunology (2007) [Pubmed]
  2. Canonical NF-kappaB activity, dispensable for B cell development, replaces BAFF-receptor signals and promotes B cell proliferation upon activation. Sasaki, Y., Derudder, E., Hobeika, E., Pelanda, R., Reth, M., Rajewsky, K., Schmidt-Supprian, M. Immunity (2006) [Pubmed]
  3. TNF cytokine family: more BAFF-ling complexities. Laâbi, Y., Egle, A., Strasser, A. Curr. Biol. (2001) [Pubmed]
  4. Genetic studies of B-lymphocyte deficiency and mastocytosis in strain A/WySnJ mice. Clise-Dwyer, K., Amanna, I.J., Duzeski, J.L., Nashold, F.E., Hayes, C.E. Immunogenetics (2001) [Pubmed]
  5. Immunology. Long live the mature B cell--a baffling mystery resolved. Waldschmidt, T.J., Noelle, R.J. Science (2001) [Pubmed]
  6. Act1, a negative regulator in CD40- and BAFF-mediated B cell survival. Qian, Y., Qin, J., Cui, G., Naramura, M., Snow, E.C., Ware, C.F., Fairchild, R.L., Omori, S.A., Rickert, R.C., Scott, M., Kotzin, B.L., Li, X. Immunity (2004) [Pubmed]
  7. BCMA is essential for the survival of long-lived bone marrow plasma cells. O'Connor, B.P., Raman, V.S., Erickson, L.D., Cook, W.J., Weaver, L.K., Ahonen, C., Lin, L.L., Mantchev, G.T., Bram, R.J., Noelle, R.J. J. Exp. Med. (2004) [Pubmed]
  8. B cells expressing Bcl-2 and a signaling-impaired BAFF-specific receptor fail to mature and are deficient in the formation of lymphoid follicles and germinal centers. Rahman, Z.S., Manser, T. J. Immunol. (2004) [Pubmed]
  9. Cutting edge: A/WySnJ transitional B cells overexpress the chromosome 15 proapoptotic Blk gene and succumb to premature apoptosis. Amanna, I.J., Clise-Dwyer, K., Nashold, F.E., Hoag, K.A., Hayes, C.E. J. Immunol. (2001) [Pubmed]
  10. Enforced bcl-xL gene expression restored splenic B lymphocyte development in BAFF-R mutant mice. Amanna, I.J., Dingwall, J.P., Hayes, C.E. J. Immunol. (2003) [Pubmed]
  11. Coupling between B cell receptor and phospholipase C-gamma2 is essential for mature B cell development. Hikida, M., Johmura, S., Hashimoto, A., Takezaki, M., Kurosaki, T. J. Exp. Med. (2003) [Pubmed]
  12. Normal induction but attenuated progression of germinal center responses in BAFF and BAFF-R signaling-deficient mice. Rahman, Z.S., Rao, S.P., Kalled, S.L., Manser, T. J. Exp. Med. (2003) [Pubmed]
  13. BAFF augments certain Th1-associated inflammatory responses. Sutherland, A.P., Ng, L.G., Fletcher, C.A., Shum, B., Newton, R.A., Grey, S.T., Rolph, M.S., Mackay, F., Mackay, C.R. J. Immunol. (2005) [Pubmed]
  14. Flow cytometric analysis of two incorporated halogenated thymidine analogues and DNA in a mouse mammary tumor grown in vivo. Pollack, A., Terry, N.H., Van, N.T., Meistrich, M.L. Cytometry. (1993) [Pubmed]
  15. B cell-activating factor belonging to the TNF family acts through separate receptors to support B cell survival and T cell-independent antibody formation. Shulga-Morskaya, S., Dobles, M., Walsh, M.E., Ng, L.G., MacKay, F., Rao, S.P., Kalled, S.L., Scott, M.L. J. Immunol. (2004) [Pubmed]
  16. Survival signaling in resting B cells. Patke, A., Mecklenbräuker, I., Tarakhovsky, A. Curr. Opin. Immunol. (2004) [Pubmed]
  17. Double knockout mice show BASH and PKCdelta have different epistatic relationships in B cell maturation and CD40-mediated activation. Nojima, T., Hayashi, K., Goitsuka, R., Nakayama, K., Nakayama, K., Kitamura, D. Immunol. Lett. (2006) [Pubmed]
  18. Effect of CBA/N xid on spontaneous production of antibodies to DNA in MRL/1 and NZB backcross mice. Cowdery, J.S., Taurog, J.D., Steinberg, A.D. Scand. J. Immunol. (1980) [Pubmed]
  19. Isolation of immunogenic and lethal peptides of alpha-toxin from Clostridium novyi type B. Schranner, I., Erhard, M.H., Kaltner, H., Lösch, U. Toxicon (1992) [Pubmed]
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