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
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