Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. “Lymphocyte homing”—the targeted migration of lymphocytes between organs—serves as the physiological foundation for immune surveillance and local immune homeostasis. Under septic conditions, this precisely regulated process is severely disrupted, leading to failed recruitment of immune cells to infection/injury sites and exacerbated depletion of lymphoid tissues, ultimately inducing systemic immune imbalance. This review elaborates on three core aspects: the physiological basis of intestinal lymphocyte homing, the mechanisms by which sepsis disrupts this pathway (including immune microenvironment remodeling, abnormal homing signaling, and regulatory T cell dysfunction), and targeted interventional strategies (chemokine receptor antagonists, integrin-directed regulation, and microbiota-immune crosstalk modulation). Understanding lymphocyte homing disorder provides a novel breakthrough for deciphering septic immunosuppression and improving clinical outcomes.
Geng et al. (Thu,) studied this question.