This is the authors' abstract. We don't add key points for this paper.
μMT knockout mice are genetically deficient in the transmembrane domain of mu chain of the immunoglobulin M (IgM) heavy chain, resulting in the absence of mature B cells.μMT knockout mice is an in vivo model system used to clarify the role of B cells in various diseases.Enteropathogenic Escherichia coli (EPEC) induces acute and chronic diarrheal disease, especially in children of developing countries.The formation of attaching and effacing (A/E) lesion is a prominent pathogenic factor in the intestinal epithelium of EPEC infection.The A/E lesion is modulated by genes located on the pathogenic island locus of enterocyte effacement (LEE) which encode a type III secretion system (T3SS) and A/E lesion-related effector proteins.Citrobacter rodentium is a murine pathogen utilized in studying the pathogenic mechanisms of EPEC in human infections.Citrobacter rodentium produce A/E lesion to attach to intestinal epithelium, thus providing a murine model pathogen to study EPEC.Several studies have investigated the pathogenesis of Citrobacter rodentium in the μMT knockout mice.In this review, we introduce the μMT murine model in the context of C. rodentium pathogenesis and describe in detail the role of B cells and antibodies in this disease.
Answers are grounded in this paper and cite their sources.
No takes yet. Share an insight, caveat, or question.
Jo et al. (2018) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: