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Immune Recognition and Response to the Renal Interstitium View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Kidney International, Vol. 31(1991), pp. 518—530 Immune recognition and response to the renal interstitium CAROLYN J. KELLY, DAVID A. ROTH, and CATHERINE M. MEYERS Renal-Electrolyte Section, University of Pennsylvania, Philadelphia, Pennsylvania, USA Advances in cellular and molecular immunology over the paststricted localization, or it may not be visible because it has not decade have revolutionized the way we think about interactionsbeen processed in such a way to be recognizable to T cells. T between the immune system and parenchymal tissues. Thecells recognize peptide fragments of antigen in association with availability of well characterized experimental models of organ-either class II (CD4 cells) or class I (CD8 cells) major specific or systemic autoimmunity has allowed advances inhistocompatibility complex (MHC) antigens [13—151. Cells basic immunology to be incorporated into understanding thewhich present antigen to class 11-restricted CD4 T cells are basis for deviant immune responses resulting in host injury, asthought to endocytose the antigen, digest it within lysosomes, well as the mechanisms of tolerance to organ-specific antigensand re-express peptide fragments of the antigen associated with [1—5]. This review outlines a framework analysis for under-class II MHC [16, 171. This antigen-MHC association probably standing how the immune system interacts with the interstitialoccurs in a peptide "groove" in the class II antigen [181, as has compartment of the kidney. This framework is comprised ofbeen demonstrated to exist on class I by crystallographic four sections. The first details requirements for the induction ofstructure [19, 20]. The effector limb of the cell-mediated nephri- immune responses, including antigen expression in the kidneytogenic immune response undoubtedly recognizes interstitial and how such antigen is presented to the immune system. Theglycoprotein antigens as peptides complexed with MHC anti- second section summarizes work from both experimental mod-gens of native renal cells, that is, tubular cells, interstitial els and human studies which have characterized cell-mediatedfibroblasts, or, perhaps, the endothelial cells of the interstitial immune responses in interstitial disease [6]. The third section isvascular network. How the afferent or inductive limb of the an update of the antibody response to interstitial antigens, ascellular nephritogenic immune response is induced in vivo is well as the role of antibody in the effector limb of the immuneless clear. There are three major possibilities. The target response, an area which has been previously reviewed exten- antigen may be presented to CD4 T helper (Th) cells by native sively [3, 4]. The final section discusses how immune responsesrenal cells (tubular cells, fibroblasts, or tissue-based macro- to interstjtial antigens are typically regulated, either by the hostphages) in association with class II MHC [21, 221. Activated Th or through external manipulations, such that tolerance to organ- cells then provide permissive help for both humoral and cell- specific antigens is maintained [7—9]. mediated effector immunity. Alternatively, the target antigen Antigen expression and presentation may be endocytosed and processed by circulating antigen- In order for an immune response targeted to interstitialpresenting cells (APCs), with T cell education occurring in the antigens to be initiated, the antigen must be expressed withinperipheral lymphoid organs instead of locally within the kidney. The third possibility is that the antigen inducing the immune the interstitial compartment of the kidney and must be immu- response is cross reactive with a kidney antigen. An infectious nologically "visible" to the immune system. Polymorphisms in target antigen expression define one level of susceptibility toagent or drug may be processed by APCs in peripheral lym- autoimmune nephritis. The target antigen of anti-tubular base-phoid organs and activate antigen-specific Th cells. The effector limb of this immune response would recognize both the stimu- ment membrane (aTBM) disease, for example, is not expressed in all inbred rodent strains or all humans [10—12]. Circulatinglating antigen as well as a cross reactive epitope expressed in immune products specific for this target antigen do not lead tothe interstitium. While this hypothesis of cross reactive anti- interstitial injury in such a host. Such polymorphisms in targetgens as the basis for autoimmunity ("molecular mimicry" [231) antigen expression underlie the occasional observation ofhas much intrinsic appeal, there is not yet supportive evidence aTBM antibodies in renal allografts which react with graft, butfor its relevance to kidney disease. not native, kidney [121. The extent to which interstitial glyco- There is experimental evidence to support the hypothesis that proteins display polymorphism, aside from this one instance, isnative renal cells can process and present antigen to T cells [21, 22, 24]. Murine proximal tubular epithelial cells (MCT) synthe- largely unexplored. Antigen visibility consists of several components in additionsize the 3M-l antigen and can present this antigen to CD4, to antigen presence in the interstitium. An antigen may not be3M-l-specific T cells [21, 25]. This interaction obeys the "rules" of classic APC-T cell interactions in that it can be blocked by routinely exposed to circulating lymphocytes because of re-aCD4 or anti-class II antibodies [26, 27]. There are several novel aspects to this interaction. APC's for class Il-restricted T cells are not typically envisioned as presenting self antigens; © 1991 by the International Society of Nephrology rather they endocytose, digest, and present exogenous antigens 518 Kelly et al: Immune system in the interstitium 519 [16, 17]. Self antigens are thought to be predominantly ex-in the context of interstitial injury. The final section will discuss pressed in the context of class I MHC molecules and recognizedT cell regulation. by CD8 T cells. This distinction has arisen in part because purified organ parenchymal cells and defined organ-specific T cell-mediated immunity in aTBM disease antigens are not widely available to test this hypothesis. Yet Although the fully developed lesion of sTBM-associated there is precedent for such a phenomenon in other systems:interstitial nephritis could not be transferred with immune cells thyroid epithelial cells can support the proliferation of thyro-alone in rats and guinea pigs, early studies demonstrated that globulin specific T cells [28]. sensitized T cells were an important component of the autoim- The other novel aspect to the MCT interaction with 3M-i-mune lesion [33—36]. The role of T cells in mediating inflamma- specific T cells is that it can be inhibited by antibodies to thetory interstitial nephritis has been most extensively character- 3M-l antigen [21]. Anti-antigen antibodies do not typicallyized in the murine model of aTBM disease. Two observations interfere with antigen presentation. The structural explanationprovided the impetus for an in-depth analysis of the T cell for this is that the antibody cannot easily interact with a peptiderepertoire in this model. The first was that there were no buried deep within a peptide "groove" in the MHC moleculedifferences in humoral immunity between immunized suscepti- [20]. There are two major possible explanations as to whyble and nonsusceptible strains of mice which could explain the a3M-1 antibodies inhibit stimulation of CD4 T cells by MCTvastly different outcomes following immunization [37]. The cells. The first is that the immunogenic peptide is not deeplysecond observation was that transfer of immune T cells into buried and is, therefore, accessible to the antibody. The othergenetically compatible naive recipients predictably results in possibility is that the antibody has an indirect effect on antigenmononuclear cell infiltration of the interstitium, progressive presentation. Recent evidence supports the latter hypothesis.fibrosis, and eventual organ failure [38]. The T cells required for Anti-3M-i antibodies decrease class II MHC antigen expressiontransfer of disease are present in the spleen and draining lymph by MCT cells in vitro and by proximal tubular epithelium innodes of syngeneic, immunized SJL mice [39]. A combination vivo [291. Nuclear run-off assays of nascent RNA transcriptsof in vivo and in vitro studies of relevant 3M-i specific T cells from MCT cells coincubated with a3M- 1 antibodies suggest thathas resulted in an integrated understanding of the events this regulatory event occurs at a transcriptional level [29].required for differentiation and function of nephritogenic T Instead of causing target cell damage, such an interactioncells. Since the disease is induced by immunization, the matu- between autoantibodies and target cell may actually ameliorateration of the T cell response can be studied from the time the intensity of cellular immune injury. This is clearly the caseantigen, in an immunogenic form, is introduced into the system. in murine aTBM disease: class Il-restricted inflammatory ef- fector T cells will mediate interstitial injury when class II Analysis of 3M-i reactive T cells in murine aTBM disease expression is heightened by gamma interferon (y-IFN) [29]. If Within several days of immunization with 3M-I, CD4 helper augmented class II expression is blocked with a3M-l antibod-T
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