investigating the importance of b cells and antibodies during trichuris muris infection using the igmi mouse

The igmi mouse has normal b cell development; its b cells express an igm b cell receptor but cannot class switch or secrete antibody. thus, the igmi mouse offers a model system by which to dissect out antibody-dependent and antibody-independent b cell function. here, we provide the first detailed characterisation of the igmi mouse post-trichuris muris (t. muris) infection, describing expulsion phenotype, cytokine production, gut pathology and changes in t regulatory cells, t follicular helper cells and germinal centre b cells, in addition to rna sequencing (rna seq) analyses of wild-type littermates (wt) and mutant b cells prior to and post infection. igmi mice were susceptible to a high-dose infection, with reduced th2 cytokines and elevated b cell-derived il-10 in mesenteric lymph nodes (mln) compared to controls. a low-dose infection regime revealed igmi mice to have significantly more apoptotic cells in the gut compared to wt mice, but no change in intestinal inflammation. il-10 levels were again elevated. collectively, this study showcases the potential of the igmi mouse as a tool for understanding b cell biology and suggests that the b cell plays both antibody-dependent and antibody-independent roles post high- and low-dose t. muris infection.