title: Inhibition of osteoclast differentiation and matrix metalloproteinase production by CD4+CD25+ T cells in mice.
abstract: To reveal the mechanism of inflammation-accompanied osteoporosis, mouse CD11b cells and CD4+CD25+ T cells were cocultured. Our results showed that CD11b+ monocytes cocultured with CD4+CD25+ T cells generated significantly less osteoclasts than those cocultured with CD4+CD25- T cells. The levels of MMP-7 and 9 in coculture supernatant were decreased significantly when CD11b+ monocytes and CD4+CD25+ T cells were cocultured comparing to the CD4+CD25- T cell group. These results highlight the role of CD4+CD25+ T cells on rheumatic osteoporosis.
  
  
  BACKGROUND
  The purpose of this study was to reveal the mechanism of inflammation-accompanied osteoporosis by examining the effect of CD4+CD25+ T cells on osteoclast formation, as well as the production of matrix metalloproteinases (MMP)-2, 3, 7, and 9 from osteoclasts.
  
  
  METHODS
  Mouse CD11b cells and CD4+CD25+ T cells were isolated using the microbead-based kits. Activated CD11b cells and CD4+CD25+ T were cocultured. CD4+CD25- T cells were used as controls. Osteoclasts were evaluated by counting the average of tartrate-resistant acid phosphatase-positive multinucleated large cells among five high-power fields (×200). After 2 days of coculture, supernatants were harvested for MMP measurement (by ELISA).
  
  
  RESULTS
  At day 7, the CD11b+ monocytes cocultured with CD4+CD25+ T cells generated significantly (both p < 0.01) less osteoclasts (3.4 ± 0.8) than those cocultured with CD4+CD25- T cells (16.2 ± 1.3) and those cultured alone (16.2 ± 2.7). The supernatant levels of MMP-7 and 9 were decreased significantly (p < 0.01) when CD11b+ monocytes and CD4+CD25+ T cells were cocultured compared to the other two conditions.
  
  
  CONCLUSIONS
  The decreased CD4+CD25+ T cells may cause an overproduction of MMP-7 and 9 from osteoclasts, which highlight the role of CD4+CD25+ T cells on rheumatic osteoporosis.
authors.affiliation: Department of Rheumatology and Immunology, First Affiliated Hospital, China Medical University, Shenyang 110001, China. yangpingting@yahoo.com
authors.forename: P T
authors.initials: PT
authors.lastname: Yang
authors.forename: X H
authors.initials: XH
authors.lastname: Meng
authors.forename: Y
authors.initials: Y
authors.lastname: Yang
authors.forename: W G
authors.initials: WG
authors.lastname: Xiao
mesh_terms: D000818:Animals; D039481:CD11b Antigen / Q000032:analysis; D002450:Cell Communication / Q000502:physiology; D002454:Cell Differentiation / Q000502:physiology; D018920:Coculture Techniques; D005260:Female; D017493:Leukocyte Common Antigens / Q000032:analysis; D020782:Matrix Metalloproteinases / Q000096:biosynthesis*; D051379:Mice; D008810:Mice, Inbred C57BL; D009000:Monocytes / Q000166:cytology*; D010010:Osteoclasts / Q000166:cytology* / Q000201:enzymology; D050378:T-Lymphocytes, Regulatory / Q000502:physiology*
chemical_list: D039481:CD11b Antigen; D017493:Leukocyte Common Antigens; C516770:Ptprc protein, mouse; D020782:Matrix Metalloproteinases