The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)



Gene Review

Tnfsf13b  -  tumor necrosis factor (ligand) superfamily...

Mus musculus

Synonyms: B-cell-activating factor, BAFF, BLyS, Baff, D8Ertd387e, ...
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of Tnfsf13b


High impact information on Tnfsf13b

  • These findings demonstrate the involvement of zTNF4 and its receptors in the development of SLE and identify TACI-Ig as a promising treatment of autoimmune disease in humans [5].
  • Transgenic animals overexpressing zTNF4 in lymphoid cells develop symptoms characteristic of systemic lupus erythaematosus (SLE) and expand a rare population of splenic B-Ia lymphocytes [5].
  • Here we report an absolute requirement for BAFF in normal B cell development [6].
  • 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.) [7].
  • Thus, both classical and alternative NF-kappaB signaling are important for development of lupus-like disease associated with BAFF overproduction [8].

Biological context of Tnfsf13b


Anatomical context of Tnfsf13b


Associations of Tnfsf13b with chemical compounds


Physical interactions of Tnfsf13b

  • Moreover, we show that, in contrast to monovalent BAFF-R-Fc, monovalent BCMA does not form stable complexes with BAFF [18].

Regulatory relationships of Tnfsf13b

  • BAFF-induced NEMO-independent processing of NF-kappa B2 in maturing B cells [19].
  • A transmembrane activator and calcium-modulating and cyclophilin ligand interactor (TACI)-Ig fusion protein (which neutralizes both BAFF and a proliferation-inducing ligand (APRIL), another TNF family member) inhibited Hg-induced autoantibody or serum IgE production [10].
  • In this study, we show that BLyS activates NF-kappaB through both classical and alternative pathways with distinct kinetics in quiescent mature B cells [20].
  • These studies clearly demonstrate that BAFF regulates Ab responses in vivo through receptors in addition to BAFF-R [21].
  • Our data suggest the existence of a previously unknown BAFF-induced and PKCdelta-mediated nuclear signalling pathway which regulates B-cell survival [22].

Other interactions of Tnfsf13b


Analytical, diagnostic and therapeutic context of Tnfsf13b

  • Using a collagen-induced arthritis (CIA) mouse model, we detected dysregulated expression of BAFF and its receptors in the peripheral lymphoid organs during arthritis induction [26].
  • By reverse transcription-polymerase chain reaction (RT-PCR), we find that gene expression of CXCL13, a chemokine involved in B-cell recruitment into lymphoid follicles, and BAFF, a key regulator of B-cell survival, is markedly and persistently upregulated in the CNS of mice with relapsing-remitting and chronic-relapsing EAE [27].
  • Using size exclusion chromatography and static light scattering to monitor trimer to 60-mer ratios in BAFF preparations, we find that 60-mer formation is pH-dependent and requires histidine 218 within the DE loop of BAFF [17].
  • In animal models of autoimmune disease, BLyS antagonists reduce disease severity and delay disease progression [28].
  • Unlike monoclonal antibodies, which have long plasma half-lives and considerable liver uptake, BLyS has distinct pharmacokinetic and biodistribution properties that may offer advantages compared with antibody-based radioimmunotherapy [29].


  1. 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]
  2. 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]
  3. Development of nephritis but not sialadenitis in autoimmune-prone BAFF transgenic mice lacking marginal zone B cells. Fletcher, C.A., Sutherland, A.P., Groom, J.R., Batten, M.L., Ng, L.G., Gommerman, J., Mackay, F. Eur. J. Immunol. (2006) [Pubmed]
  4. In vitro and in vivo activation induces BAFF and APRIL expression in B cells. Chu, V.T., Enghard, P., Riemekasten, G., Berek, C. J. Immunol. (2007) [Pubmed]
  5. TACI and BCMA are receptors for a TNF homologue implicated in B-cell autoimmune disease. Gross, J.A., Johnston, J., Mudri, S., Enselman, R., Dillon, S.R., Madden, K., Xu, W., Parrish-Novak, J., Foster, D., Lofton-Day, C., Moore, M., Littau, A., Grossman, A., Haugen, H., Foley, K., Blumberg, H., Harrison, K., Kindsvogel, W., Clegg, C.H. Nature (2000) [Pubmed]
  6. An essential role for BAFF in the normal development of B cells through a BCMA-independent pathway. Schiemann, B., Gommerman, J.L., Vora, K., Cachero, T.G., Shulga-Morskaya, S., Dobles, M., Frew, E., Scott, M.L. Science (2001) [Pubmed]
  7. Immunology. Long live the mature B cell--a baffling mystery resolved. Waldschmidt, T.J., Noelle, R.J. Science (2001) [Pubmed]
  8. Alternative and Classical NF-kappaB Signaling Retain Autoreactive B Cells in the Splenic Marginal Zone and Result in Lupus-like Disease. Enzler, T., Bonizzi, G., Silverman, G.J., Otero, D.C., Widhopf, G.F., Anzelon-Mills, A., Rickert, R.C., Karin, M. Immunity (2006) [Pubmed]
  9. Homeostatic cell-cycle control by BLyS: Induction of cell-cycle entry but not G1/S transition in opposition to p18INK4c and p27Kip1. Huang, X., Di Liberto, M., Cunningham, A.F., Kang, L., Cheng, S., Ely, S., Liou, H.C., Maclennan, I.C., Chen-Kiang, S. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  10. A role for B cell-activating factor of the TNF family in chemically induced autoimmunity. Zheng, Y., Gallucci, S., Gaughan, J.P., Gross, J.A., Monestier, M. J. Immunol. (2005) [Pubmed]
  11. 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]
  12. Extracellular proteinase inhibitor-accelerated apoptosis is associated with B cell activating factor in mammary epithelial cells. Jung, D.J., Bong, J.J., Baik, M. Exp. Cell Res. (2004) [Pubmed]
  13. Unique CD40-mediated biological program in B cell activation requires both type 1 and type 2 NF-kappaB activation pathways. Zarnegar, B., He, J.Q., Oganesyan, G., Hoffmann, A., Baltimore, D., Cheng, G. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  14. Activation and accumulation of B cells in TACI-deficient mice. Yan, M., Wang, H., Chan, B., Roose-Girma, M., Erickson, S., Baker, T., Tumas, D., Grewal, I.S., Dixit, V.M. Nat. Immunol. (2001) [Pubmed]
  15. Reactive oxygen species augment B-cell-activating factor expression. Moon, E.Y., Lee, J.H., Oh, S.Y., Ryu, S.K., Kim, H.M., Kwak, H.S., Yoon, W.K. Free Radic. Biol. Med. (2006) [Pubmed]
  16. BAFF regulates B cell survival by downregulating the BH3-only family member Bim via the ERK pathway. Craxton, A., Draves, K.E., Gruppi, A., Clark, E.A. J. Exp. Med. (2005) [Pubmed]
  17. Formation of virus-like clusters is an intrinsic property of the tumor necrosis factor family member BAFF (B cell activating factor). Cachero, T.G., Schwartz, I.M., Qian, F., Day, E.S., Bossen, C., Ingold, K., Tardivel, A., Krushinskie, D., Eldredge, J., Silvian, L., Lugovskoy, A., Farrington, G.K., Strauch, K., Schneider, P., Whitty, A. Biochemistry (2006) [Pubmed]
  18. Comparison of soluble decoy IgG fusion proteins of BAFF-R and BCMA as antagonists for BAFF. Pelletier, M., Thompson, J.S., Qian, F., Bixler, S.A., Gong, D., Cachero, T., Gilbride, K., Day, E., Zafari, M., Benjamin, C., Gorelik, L., Whitty, A., Kalled, S.L., Ambrose, C., Hsu, Y.M. J. Biol. Chem. (2003) [Pubmed]
  19. BAFF-induced NEMO-independent processing of NF-kappa B2 in maturing B cells. Claudio, E., Brown, K., Park, S., Wang, H., Siebenlist, U. Nat. Immunol. (2002) [Pubmed]
  20. NF-kappa B1 p50 is required for BLyS attenuation of apoptosis but dispensable for processing of NF-kappa B2 p100 to p52 in quiescent mature B cells. Hatada, E.N., Do, R.K., Orlofsky, A., Liou, H.C., Prystowsky, M., MacLennan, I.C., Caamano, J., Chen-Kiang, S. J. Immunol. (2003) [Pubmed]
  21. 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]
  22. Regulation of B-cell survival by BAFF-dependent PKCdelta-mediated nuclear signalling. Mecklenbräuker, I., Kalled, S.L., Leitges, M., Mackay, F., Tarakhovsky, A. Nature (2004) [Pubmed]
  23. BAFF/BLyS receptor 3 binds the B cell survival factor BAFF ligand through a discrete surface loop and promotes processing of NF-kappaB2. Kayagaki, N., Yan, M., Seshasayee, D., Wang, H., Lee, W., French, D.M., Grewal, I.S., Cochran, A.G., Gordon, N.C., Yin, J., Starovasnik, M.A., Dixit, V.M. Immunity (2002) [Pubmed]
  24. B cell maturation antigen, the receptor for a proliferation-inducing ligand and B cell-activating factor of the TNF family, induces antigen presentation in B cells. Yang, M., Hase, H., Legarda-Addison, D., Varughese, L., Seed, B., Ting, A.T. J. Immunol. (2005) [Pubmed]
  25. APRIL-deficient mice have normal immune system development. Varfolomeev, E., Kischkel, F., Martin, F., Seshasayee, D., Wang, H., Lawrence, D., Olsson, C., Tom, L., Erickson, S., French, D., Schow, P., Grewal, I.S., Ashkenazi, A. Mol. Cell. Biol. (2004) [Pubmed]
  26. Expression and function of TNF family member B cell-activating factor in the development of autoimmune arthritis. Zhang, M., Ko, K.H., Lam, Q.L., Lo, C.K., Srivastava, G., Zheng, B., Lau, Y.L., Lu, L. Int. Immunol. (2005) [Pubmed]
  27. Intracerebral expression of CXCL13 and BAFF is accompanied by formation of lymphoid follicle-like structures in the meninges of mice with relapsing experimental autoimmune encephalomyelitis. Magliozzi, R., Columba-Cabezas, S., Serafini, B., Aloisi, F. J. Neuroimmunol. (2004) [Pubmed]
  28. BLyS--an essential survival factor for B cells: basic biology, links to pathology and therapeutic target. Baker, K.P. Autoimmunity reviews. (2004) [Pubmed]
  29. Rapid and specific targeting of 125I-labeled B lymphocyte stimulator to lymphoid tissues and B cell tumors in mice. Riccobene, T.A., Miceli, R.C., Lincoln, C., Knight, Y., Meadows, J., Stabin, M.G., Sung, C. J. Nucl. Med. (2003) [Pubmed]
WikiGenes - Universities