Study of the immunopathogenesis of tubulointerstitial nephritis using model systems

Tubulointerstitial nephritis (TIN), as studied experimentally, can be induced by many of the same humoral immune mechanisms now recognized to cause immune forms of glomerular injury [reviewed in 1–5] (Table 1). In addition, there is compelling evidence of direct cellular immune involvement in some forms of TIN. In general, however, less is known about the immunopathogenesis of human TIN than its glomerular counterpart. For example, the specific mechanisms responsible for many of the instances of TIN associated with drug hypersensitivity remain unclear. Much of what is known comes from the study of experimental models of TIN. In addition, these model systems are being used to forward the understanding of control of nephritogenic immune reactions [6–10]. This paper will focus on a discussion of the different immune mechanisms that have been shown to contribute to TIN in experimental models and their extension to human TIN as appropriate