Author: ["Maria-Teresa Ochoa","Steffen Stenger","Peter A. Sieling","Sybille Thoma-Uszynski","Shereen Sabet","Sungae Cho","Alan M. Krensky","Martin Rollinghoff","Euzenir Nunes Sarno","Anne E. Burdick","Thomas H. Rea","Robert L. Modlin"]
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Abstract
A novel mechanism by which T cells contribute to host defense against microbial pathogens is release of the antimicrobial protein granulysin. We investigated the role of granulysin in human infectious disease using leprosy as a model. Granulysin-expressing T cells were detected in cutaneous leprosy lesions at a six-fold greater frequency in patients with the localized tuberculoid as compared with the disseminated lepromatous form of the disease. In contrast, perforin, a cytolytic molecule that colocalizes with granulysin in cytotoxic granules, was expressed at similar levels across the spectrum of disease. Within leprosy lesions, granulysin colocalized in CD4+ T cells and was expressed in CD4+ T-cell lines derived from skin lesions. These CD4+ T-cell lines lysed targets by the granule exocytosis pathway and reduced the viability of mycobacteria in infected targets. Given the broad antimicrobial spectrum of granulysin, these data provide evidence that T-cell release of granulysin contributes to host defense in human infectious disease.Cite this article
Ochoa, MT., Stenger, S., Sieling, P. et al. T-cell release of granulysin contributes to host defense in leprosy. Nat Med 7, 174–179 (2001). https://doi.org/10.1038/84620 