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Increased susceptibility to oral Trichuris muris infection in the specific absence of CXCR 5 + CD 11c + cells
Author(s) -
Bradford Barry M.,
Donaldson David S.,
Forman Ruth,
Else Kathryn J.,
Mabbott Neil A.
Publication year - 2018
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/pim.12566
Subject(s) - biology , cd11c , cxcr5 , immunology , immune system , interleukin 17 , cxcl13 , acquired immune system , chemokine , t cell , microbiology and biotechnology , chemokine receptor , phenotype , biochemistry , gene
Summary 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)‐polarized immune response. Susceptible mouse strains, in contrast, mount an inappropriate Th1 response to T. muris infection. Expression of the chemokine CXCL 13 by stromal follicular dendritic cells attracts CXCR 5‐expressing cells towards the B‐cell follicles. Previous studies using a complex in vivo depletion model have suggested that CXCR 5‐expressing conventional dendritic cells ( cDC ) help regulate the induction of Th2‐polarized responses. Here, transgenic mice with CXCR 5 deficiency specifically restricted to CD 11c + cells were used to determine whether the specific absence CXCR 5 on CD 11c + 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 CXCR 5 expression on CD 11c + cells failed to clear T. muris infection and developed cytokine and antibody responses that suggested a disturbed Th1/Th2 balance with enhanced IFN ‐γ expression. These data suggest an important role of CXCR 5‐expressing CD 11c + cells such as cDC in immunity to oral T. muris infection.