Upon contact with live trypanosomes parasites, B immune cells in mice release interleukin 17 (IL-17) that confers protection in response to this infection according to a report published online in Nature Immunology this week.
Infection with the parasite Trypanosoma cruzi elicits robust inflammatory responses that, if unchecked, can lead to immune cell-mediated tissue damage and wasting disease. David Rawlings and colleagues show that B cells exposed to an enzyme released by T. cruzi, trans-sialidase, trigger the expression of IL-17, an immune system mediator that acts to recruit neutrophils-the most abundant type of white blood cells. Mice that harbor IL-17-deficient B cells exhibit more severe liver damage and reduced survival rate due to an inability to control trypanosome infections as compared to normal mice, suggesting that B cell production of IL-17 is crucial.
The authors further discover that B cells utilize a completely different signaling cascade to initiate IL-17 expression, triggered by trans-sialylation of the surface molecule CD45 on B cells. Human B cells also produce IL-17 in response to trans-sialidase.
These findings suggest B cells play additional roles to combat parasite infection beyond their production of antibodies, which may be important for controlling other pathogens that express trans-sialidase. It also raises the question of whether some autoimmune syndromes, lupus, linked to B cells might exhibit dysregulated expression of IL-17.
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