CO-stimulatory molecules can assist in augmenting heat shock induced APC function

T cell activation occurs following the recognition of la/antigen complexes on APCs and in conjunction with biding of co-stimulatory and adhesion molecules such as B7 and ICAM. The heat shock response is present in many cell types, including lymphocytes. It is characterized by the synthesis of heat shock proteins, that can alter normal sub-cellular regulatory pathways in order to enhance survival from stressful conditions that occur, for example, by exposure to increased temperatures. The present studies were initiated to determine whether heat shock can be adapted to alter APC function and thereby increase T cell responses. LB27.4, a B cell APC line, was exposed to hyperthermic or normal temperature conditions and co-cultured with the D10.G4 helper T cell line. Our results indicate that heat shock can enhance the ability of APCs to activate both T cell proliferation and IL secretion. The co-stimulatory molecule, B7-2 and the adhesion molecule ICAM are responsible, at least in part, for the activation of APC function. Increased function occurs concomitantly with synthesis of heat shock proteins and increased adhesive properties. The use of physiologic stress may provide insight into normal immune regulation and may have therapeutic implications in disease management. Supported by the NIH and Hoechst-Celanese Innovative Research Award.