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Summary  Healthy host–microbe mutualism relies on compartmentalization and proper regulation of systemic and mucosal immune responses. Nevertheless, the systemic immune system is frequently exposed to bouts of bacteraemia, which can trigger systemic antimicrobial immune reactivity including  CD 4 +  T cells. Low‐level bacteraemia can occur when immune compartmentalization is compromised, for example in the presence of innate immune deficiency or following use of non‐steroidal anti‐inflammatory drugs. We generated an  Escherichia coli  strain expressing a defined T helper neo‐epitope to study systemic antigen‐specific antimicrobial  CD 4 +  T cells and their potential involvement in the pathogenisis of inflammatory bowel diseases. We found that the dose of bacteria required for the induction of systemic antimicrobial  CD 4 +  T‐cell proliferation was high and not easily reached under physiological conditions. Importantly, however, when intestinal barrier function was compromised by induced damage to the intestinal epithelium, the presence of systemic antimicrobial  CD 4 +  T cells specific for a single neo‐antigen resulted in dramatically increased levels of bacterial translocation. This study therefore demonstrates that systemic antimicrobial  CD 4 +  T‐cell reactivity might impact adversely on the mucosa under conditions of reduced barrier function and that despite strong mucosal immune regulation, antigen‐specific recognition is still sensitive.

Detrimental effect of systemic antimicrobial CD 4 + T‐cell reactivity on gut epithelial integrity