“…However, the specific mediators or the minimal threshold required to initiate a stress reaction are not known. Some of the known local effects of cytokines (in terleukins, tumor necrosis factors, interferons, prostaglan dins) include vasoconstriction or vasodilatation, heat pro duction, and release of oxygen radicals inducing and pro moting cellular immunologic reactions, thus injuring the cells directly or indirectly [26], Furthermore, human stress proteins have been localized immunohistochcmically with monoclonal antibodies to HSP 69 and 70 with in synovial cells, infiltrating inflammatory cells, and dis eased cartilage cells in joint tissues obtained from patients with arthritis [ 12,13]. HSP 70 was also demonstrated in normal and atherosclerotic specimens of the aorta and in plaque-associated macrophages, more so in the areas of necrosis, probably secondary to ischemia or release of cytokines [14], An interesting finding in our study is the enhanced expression of HSP only in those segments of the nephron that are surrounded by active interstitial inflammation.…”