A novel and divergent role of granzyme A and B in resistance to helminth infection

Wiebke Hartmann, Benjamin J. Marsland, Benjamin Otto, Jens Urny, Bernhard Fleischer, Simone Korten

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14 Citations (Scopus)


Granzyme (gzm) A and B, proteases of NK cells and T killer cells, mediate cell death, but also cleave extracellular matrices, inactivate intracellular pathogens, and induce cytokines. Moreover, macrophages, Th2cells, regulatory T cells, mast cells, and B cells can express gzms. We recently reported gzm induction in human filarial infection. In this study, we show that in rodent filarial infection with Litomosoides sigmodontis, worm loads were significantly reduced in gzmAxB and gzmB knockout mice during the whole course of infection, but enhanced only early in gzmA knockout compared with wild-type mice. GzmA/B deficiency was associated with a defense-promoting Th2 cytokine and Ab shift, enhanced early inflammatory gene expression, and a trend of reduced alternatively activated macrophage induction, whereas gzmA deficiency was linked with reduced inflammation and a trend toward increased alternatively activated macrophages. This suggests a novel and divergent role for gzms in helminth infection, with gzmA contributing to resistance and gzmB promoting susceptibility.

Original languageEnglish
Pages (from-to)2472-2481
Number of pages10
JournalJournal of Immunology
Issue number4
Publication statusPublished - 15 Feb 2011
Externally publishedYes

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