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Soluble glucocorticoid-induced tumor necrosis factor receptor (sGITR) stimulates osteoclast differentiation in response to receptor activator of NF-κB ligand (RANKL) in osteoclast cells
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Functional impairment of CD8+ T cells by regulatory T cells during persistent retroviral infection
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TCR-mediated activation promotes GITR upregulation in T cells and resistance to glucocorticoid-induced death
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GITR activation induces an opposite effect on alloreactive CD4+ and CD8+ T cells in graft-versus-host disease
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