A novel and divergent role of granzyme A and B in resistance to helminth infection.
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A novel and divergent role of granzyme A and B in resistance to helminth infection. / Hartmann, Wiebke; Marsland, Benjamin J; Otto, Benjamin; Urny, Jens; Fleischer, Bernhard; Korten, Simone.
In: J IMMUNOL, Vol. 186, No. 4, 4, 2011, p. 2472-2481.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - A novel and divergent role of granzyme A and B in resistance to helminth infection.
AU - Hartmann, Wiebke
AU - Marsland, Benjamin J
AU - Otto, Benjamin
AU - Urny, Jens
AU - Fleischer, Bernhard
AU - Korten, Simone
PY - 2011
Y1 - 2011
N2 - 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, Th2 cells, 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 gzmA × B 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.
AB - 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, Th2 cells, 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 gzmA × B 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.
M3 - SCORING: Zeitschriftenaufsatz
VL - 186
SP - 2472
EP - 2481
JO - J IMMUNOL
JF - J IMMUNOL
SN - 0022-1767
IS - 4
M1 - 4
ER -
