OSTEOCLAST DIFFERENTIATION ANTIGEN

Authors
Citation
T. Kukita et A. Kukita, OSTEOCLAST DIFFERENTIATION ANTIGEN, Histology and histopathology, 11(3), 1996, pp. 821-830
Citations number
94
Categorie Soggetti
Cell Biology
ISSN journal
02133911
Volume
11
Issue
3
Year of publication
1996
Pages
821 - 830
Database
ISI
SICI code
0213-3911(1996)11:3<821:ODA>2.0.ZU;2-2
Abstract
Osteoclasts are the primary cells which perform bone resorption. The o rigin of these multi-nucleated giant cells is the haematopoietic stem cells. The differentiation pathway of the osteoclasts has so far been well studied and the cell-lineage of these bone resorbing cells is con sidered to be close but not identical to the monocytes/macrophages. Ow ing to the development of in vitro culture systems for evaluating oste oclast differentiation, it has been elucidated that various cytokines are involved in the differentiation of the osteoclasts. However, there is still ambiguity concerning the molecular mechanism of the differen tiation of the osteoclasts. One approach for clarifying the molecular mechanism is to find unique antigen molecules involved in the process of osteoclast differentiation. In this review article, we introduce su ch immunological studies concerning osteoclast differentiation. We als o refer to our recent establishment of a panel of monoclonal antibodie s recognizing rat osteoclasts. One of the monoclonal antibodies recogn izes cell surface antigen (Kat1-antigen) expressed on cells in osteocl ast-lineage and not on monocytes/macrophages. Cross-linking of the cel l surface antigen using this monoclonal antibody showed that the Kat1- antigen is the unique cell surface molecule involved in the regulation of the affinity of the calcitonin receptor and also involved in the m odulation of the bone resorption. In this review article, we overview, the current issues which should be elucidated for understanding the d ifferentiation and activation of the osteoclasts. We further emphasize the utility of the immunological approach for solving these current t arget issues.