Abstract
T-lymphocytes contribute to osteolysis in rheumatic diseases through their production of the osteoclastogenic cytokine RANKL. Mitogenic stimulation of lymphocytes has been shown to induce expression of RANKL; however, the extracellular events leading to its production have not been identified.
Highlights
RANKL expression in human T-lymphocytes requires cooperative signaling through the T-cell receptor and adhesion molecule CD2
T-lymphocytes contribute to osteolysis in rheumatic diseases through their production of the osteoclastogenic cytokine RANKL
Mitogenic stimulation of lymphocytes has been shown to induce expression of RANKL; the extracellular events leading to its production have not been identified
Summary
T-lymphocytes contribute to osteolysis in rheumatic diseases through their production of the osteoclastogenic cytokine RANKL. Mitogenic stimulation of lymphocytes has been shown to induce expression of RANKL; the extracellular events leading to its production have not been identified. Aim We sought to determine whether cell-to-cell interactions through adhesion molecules such as lymphocyte function-associated antigen 2 (CD2) were necessary to promote RANKL secretion from T-cells
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.