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Immunologically-mediated toxin-induced renal disease

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Clinical Nephrotoxins

Conclusion

There is still a long way to go before all the mechanisms responsible for drug-induced immune kidney lesions will be explained. However, the notion that T-cell activation in addition to T-cell receptor-MHC peptide interactions also requires a tissue environment is an important concept for better understanding immunopathogenic mechanisms. For example, it is noteworthy that a toxic effect of the drugs on the kidney may initiate an immune response because they promote the presentation of haptenized determinants or even of self-peptides in inflammatory conditions. Th1 cells and probably Th2 cells may be pathogenic even if the effectors responsible for the lesions may be different. For example, in some patients, eosinophils, probably activated by Th2 cells could be pathogenic. Some drugs, such as hydralazine or heavy metals behave as T-cell polyclonal activators, which is sufficient for, or contributes to, the development of autoimmunity at least in some genetic backgrounds.

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Pelletier, L., Savignac, M., Druet, P. (2003). Immunologically-mediated toxin-induced renal disease. In: de Broe, M.E., Porter, G.A., Bennett, W.M., Verpooten, G.A. (eds) Clinical Nephrotoxins. Springer, Dordrecht. https://doi.org/10.1007/1-4020-2586-6_4

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