Open AccessGamma Interferon Positively ModulatesActinobacillus actinomycetemcomitans-Specific RANKL+CD4+Th-Cell-Mediated Alveolar Bone Destruction In Vivo
Author(s) -
Yen-Tung A. Teng,
Deeqa Mahamed,
Bhagirath Singh
Publication year - 2005
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.73.6.3453-3461.2005
Subject(s) - rankl , nod , interferon gamma , biology , immunology , cancer research , periodontitis , in vivo , medicine , cytokine , activator (genetics) , receptor , biochemistry , microbiology and biotechnology
Recent studies have shown the biological and clinical significance of signaling pathways of osteogenic cytokines RANKL-RANK/OPG in controlling osteoclastogenesis associated with bone pathologies, including rheumatoid arthritis, osteoporosis, and other osteolytic disorders. In contrast to the inhibitory effect of gamma interferon (IFN-gamma) on RANKL-mediated osteoclastogenesis reported recently, alternative new evidence is demonstrated via studies of experimental periodontitis using humanized NOD/SCID and diabetic NOD mice and clinical human T-cell isolates from diseased periodontal tissues, where the presence of increasing IFN-gamma is clearly associated with (i) enhanced Actinobacillus actinomycetemcomitans-specific RANKL-expressing CD4(+) Th cell-mediated alveolar bone loss during the progression of periodontal disease and (ii) a concomitant and significantly increased coexpression of IFN-gamma in RANKL(+) CD4(+) Th cells. Therefore, there are more complex networks in regulating RANKL-RANK/OPG signaling pathways for osteoclastogenesis in vivo than have been suggested to date.