The RP105/MD-1 complex: molecular signaling mechanisms and pathophysiological implications

Schultz, Thomas E. and Blumenthal, Antje (2017) The RP105/MD-1 complex: molecular signaling mechanisms and pathophysiological implications. Journal of Leukocyte Biology, 101 1: 183-192. doi:10.1189/jlb.2VMR1215-582R


Author Schultz, Thomas E.
Blumenthal, Antje
Title The RP105/MD-1 complex: molecular signaling mechanisms and pathophysiological implications
Journal name Journal of Leukocyte Biology   Check publisher's open access policy
ISSN 1938-3673
0741-5400
Publication date 2017-01-01
Year available 2016
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1189/jlb.2VMR1215-582R
Open Access Status Not yet assessed
Volume 101
Issue 1
Start page 183
End page 192
Total pages 10
Place of publication Bethesda, MD, United States
Publisher Federation of American Societies for Experimental Biology
Language eng
Abstract Radioprotective 105 kDa (CD180) is an unusual TLR that lacks an intracellular Toll-IL-1R signaling domain and exhibits unconventional homodimerization behavior. Differential expression and functions of radioprotective 105 kDa have been associated with immune-mediated pathologies, including infection, chronic inflammation, and autoimmune disorders. Radioprotective 105 kDa activates macrophages and B cells independently of canonical TLR signaling. Current understanding of the functional consequences of radioprotective 105 kDa signaling in B cells, macrophages, and dendritic cells indicates overlapping, but also some apparent opposing, cell-specific roles for radioprotective 105 kDa in shaping cellular functions. This review compares interactions of radioprotective 105 kDa with its coreceptors, CD19, TLR4, and TLR2; integrates recent, novel findings on radioprotective 105 kDa-mediated molecular signaling mechanisms; and summarizes current understanding of its contributions to infectious, inflammatory, and autoimmune disease.
Keyword Autoimmunity
B cells
Infection
Inflammation
Macrophages
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collections: HERDC Pre-Audit
Institute for Molecular Bioscience - Publications
UQ Diamantina Institute Publications
Admin Only - UQ Diamantina Institute
 
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