Title of article :
Impaired antigen-induced CD8+ T cell clonal expansion in aging is due to defects in antigen presenting cell function
Author/Authors :
Plowden، نويسنده , , Julie and Renshaw-Hoelscher، نويسنده , , Mary and Gangappa، نويسنده , , Shivaprakash and Engleman، نويسنده , , Carrie and Katz، نويسنده , , Jacqueline M. and Sambhara، نويسنده , , Suryaprakash، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2004
Abstract :
CD8+ T cell activation depends on interaction with antigen-presenting cells (APCs) and this interaction leads to the expansion of T cells with the capacity to control infection. Using professional APCs, we demonstrate that with age, the duration of APC–T cell contact time required to achieve clonal expansion increases. Naı¨ve CD8+ T cells from aged mice showed no defect in antigen-induced proliferation when stimulated with APC from young mice. In contrast, CD8+ T cells from young mice exhibited reduced clonal expansion and secreted significantly lower amounts of IFN-γ when stimulated by APCs from aged mice. The aged APCs were defective in costimulatory molecule expression and cytokine and chemokine secretion. These data indicate that defects in APC function lead to poor T cell clonal expansion and function in aging.
Keywords :
Antigen presentation/processing , Rodent , aging , macrophages , T lymphocytes , Costimulation
Journal title :
Cellular Immunology
Journal title :
Cellular Immunology