NDLI: Decoy receptor 3 suppresses TLR2-mediated B cell activation by targeting NF-κB.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kang, Jhi-Kai Tseng, Tz-Hau Tai, Shyh-Kuan Leu, Chuen-Miin Huang, Zi-Ming Chen, Chih-Yu Hsieh, Shie-Liang Chang, Chien-Wen Chang, Yung-Chi
Description	Country affiliation: Taiwan Author Affiliation: Huang ZM ( Institute of Microbiology and Immunology, National Yang-Ming University, Taipei 11221, Taiwan.)
Abstract	Decoy receptor 3 (DcR3) is a soluble protein in the TNFR superfamily. Its known ligands include Fas ligand, homologous to lymphotoxin, showing inducible expression, and competing with HSV glycoprotein D for herpes virus entry mediator, a receptor expressed by T lymphocytes, TNF-like molecule 1A, and heparan sulfate proteoglycans. DcR3 has been reported to modulate the functions of T cells, dendritic cells, and macrophages; however, its role in regulating B cell activation is largely unknown. In this study, we found that the DcR3.Fc fusion protein bound to human and mouse B cells and suppressed the activation of B cells. DcR3.Fc attenuated Staphylococcus aureus, IgM-, Pam(3)CSK(4)-, and LPS-mediated B cell proliferation but did not affect cytokine-induced B cell growth. In the presence of these mitogens, DcR3.Fc did not induce B cell apoptosis, suggesting that DcR3 may inhibit the signal(s) important for B cell activation. Because the combination of Fas.Fc, LT-ßR.Fc (homologous to lymphotoxin, showing inducible expression, and competing with HSV glycoprotein D for herpes virus entry mediator, a receptor expressed by T lymphocytes receptor), and DR3.Fc (TNF-like molecule 1A receptor) did not suppress B cell proliferation and because the biological effect of DcR3.Fc on B cells was not blocked by heparin, we hypothesize that a novel ligand(s) of DcR3 mediates its inhibitory activity on B cells. Moreover, we found that TLR2-stimulated NF-κB p65 activation and NF-κB-driven luciferase activity were attenuated by DcR3.Fc. The TLR2-induced cytokine production by B cells was consistently reduced by DcR3. These results imply that DcR3 may regulate B cell activation by suppressing the activation of NF-κB.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	12
Volume Number	188
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-06-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	B-lymphocytes Immunology Lymphocyte Activation Nf-kappa B Receptors, Tumor Necrosis Factor, Member 6b Toll-like Receptor 2 Animals Apoptosis Metabolism Cell Proliferation Cells, Cultured Mice Real-time Polymerase Chain Reaction Recombinant Fusion Proteins Reverse Transcriptase Polymerase Chain Reaction Signal Transduction Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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