| First Author | Bradford BM | Year | 2018 |
| Journal | Parasite Immunol | Pages | e12566 |
| PubMed ID | 29920694 | Mgi Jnum | J:262182 |
| Mgi Id | MGI:6161939 | Doi | 10.1111/pim.12566 |
| Citation | Bradford BM, et al. (2018) Increased susceptibility to oral Trichuris muris infection in the specific absence of CXCR5(+) CD11c(+) cells. Parasite Immunol :e12566 |
| abstractText | Trichuris muris is a natural mouse helminth pathogen which establishes infection specifically in the caecum and proximal colon. The rapid expulsion of T. muris in resistant mouse strains is associated with the induction of a protective T helper cell type 2 (Th2)-polarised immune response. Susceptible mouse strains, in contrast, mount an inappropriate Th1 response to T. muris infection. Expression of the chemokine CXCL13 by stromal follicular dendritic cells attracts CXCR5-expressing cells towards the B cell follicles. Previous studies using a complex in vivo depletion model have suggested that CXCR5-expressing conventional dendritic cells (cDC) help regulate the induction of Th2-polarized responses. Here, transgenic with CXCR5-deficiency specifically restricted to CD11c(+) cells were used to determine whether the specific absence CXCR5 on CD11c(+) cells such as cDC would influence susceptibility to oral T. muris infection by affecting the Th1/Th2 balance. We show that in contrast to control mice, those which lacked CXCR5-expression on CD11c(+) cells failed to clear T. muris infection and developed cytokine and antibody responses that suggested a disturbed Th1/Th2 balance with enhanced IFN-gamma expression. These data suggest an important role for CXCR5-expressing CD11c(+) cells such as cDC in immunity to oral T. muris infection. This article is protected by copyright. All rights reserved. |
