First Author | Horsnell WG | Year | 2013 |
Journal | PLoS Pathog | Volume | 9 |
Issue | 10 | Pages | e1003662 |
PubMed ID | 24204255 | Mgi Jnum | J:247293 |
Mgi Id | MGI:5918077 | Doi | 10.1371/journal.ppat.1003662 |
Citation | Horsnell WG, et al. (2013) IL-4Ralpha-associated antigen processing by B cells promotes immunity in Nippostrongylus brasiliensis infection. PLoS Pathog 9(10):e1003662 |
abstractText | 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-4Ralpha and IL-13; but not IL-4. Protection did not associate with parasite specific antibody responses. Re-infection of B cell-specific IL-4Ralpha(-)/(-) 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-4Ralpha expressing B cells into naive BALB/c mice, but not IL-4Ralpha 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-4Ralpha-responsive B cells producing IL-13 contribute significantly to CD4(+) T cell-mediated protective immunity against N. brasiliensis infection. |