EFFECT OF TUMOR-DERIVES FACTORS ON SPLENIC CELL RECEPTOR MODULATION

Abstract

Natural Killer (NK) cells have natural capacity to kill tumor cell. They do not require prior antigenic sensitization and is capable of dealing with broad range of virus infected cells. Thus, NK cells play important role in host defense against tumor cells as well as virus infected cell. The sensitivity of infected cell to NK cell lysis may open new prospectives for NK cell-based immunotherapy. NK cell activation and function are strongly influenced by the interplay between inhibitory and activating signals. Tumors have evolved various mechanisms by which they can evade NK cell attack. These mechanisms include interference with NK cell activation, inhibition as well as modulation of NK cell function. The modulation may be of recognition and inhibition in NK cell receptor and modulation of co-stimulation, adhesion or susceptibility to apoptosis. Co-culturing of different cell line,one is resistant (P815) and another is sensitive (YAC-1) with the purified NK cell recovered from spleenocytes of C57BL/6 mice strain. Modulation caused in NK cell receptor was analyzed and profiled by the use of flow-cytometric methods. We found that tumor cells inhibited major NK cell receptors expression which are responsible to intiate and stimulate their immune function, including NK 1.1(mouse) inturn activate some inhibitory receptor expression which include Ly49A and Ly49C of NK cell against NK resistant cell lines.