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Ochoa, M.T. et al.

T-cell release of granulysin contributes to host defense in leprosy.

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.[1]

References

T-cell release of granulysin contributes to host defense in leprosy. Ochoa, M.T., Stenger, S., Sieling, P.A., Thoma-Uszynski, S., Sabet, S., Cho, S., Krensky, A.M., Rollinghoff, M., Nunes Sarno, E., Burdick, A.E., Rea, T.H., Modlin, R.L. Nat. Med. (2001) [Pubmed]

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