Abstract
In this study, B cell function in protective T(H)2 immunity against N. brasiliensis infection was investigated. Protection against secondary infection depended on IL-4R alpha and IL-13; but not IL-4. Protection did not associate with parasite specific antibody responses. Re-infection of B cell-specific IL-4R alpha(-/-) mice resulted in increased worm burdens compared to control mice, despite their equivalent capacity to control primary infection. Impaired protection correlated with reduced lymphocyte IL-13 production and B cell MHC class II and CD86 surface expression. Adoptive transfer of in vivo N. brasiliensis primed IL-4R alpha expressing B cells into naive BALB/c mice, but not IL-4R alpha or IL-13 deficient B cells, conferred protection against primary N. brasiliensis infection. This protection required MHC class II compatibility on B cells suggesting cognate interactions by B cells with CD4(+) T cells were important to co-ordinate immunity. Furthermore, the rapid nature of these protective effects by B cells suggested non-BCR mediated mechanisms, such as via Toll Like Receptors, was involved, and this was supported by transfer experiments using antigen pulsed Myd88(-/-) B cells. These data suggest TLR dependent antigen processing by IL-4R alpha-responsive B cells producing IL-13 contribute significantly to CD4(+) T cell-mediated protective immunity against N. brasiliensis infection.
Original language | English |
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Article number | 1003662 |
Number of pages | 12 |
Journal | PLoS Pathogens |
Volume | 9 |
Issue number | 10 |
DOIs | |
Publication status | Published - Oct 2013 |
Keywords / Materials (for Non-textual outputs)
- ALTERNATIVELY ACTIVATED MACROPHAGES
- T-CELLS
- NEMATODE PARASITES
- HELMINTH INFECTION
- PROTECTIVE IMMUNITY
- TYPE-2 IMMUNITY
- CUTTING EDGE
- RESPONSES
- MEMORY
- SALMONELLA