Abstract
<jats:sec> <jats:title>Introduction</jats:title> <jats:p>In colorectal cancer (CRC), mast cells (MCs) modulate tumor and immune cell interactions, influencing patient prognosis, though their role remains not fully elucidated. Our group previously uncovered that in the intestine MCs provide support for the effector functions of B cells, both in physiology and inflammation.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods</jats:title> <jats:p>In this work we investigated the relationship between the activation of MCs in CRC and recruitment and accumulation of B cells in the tumor environment.</jats:p> </jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p> We observed infiltration of both B cells and MCs in the tumor tissue and uncovered accumulation of CCR6 <jats:sup>+</jats:sup> B cells in tumor lymph nodes (LNs), both in the mouse model and in human patients. Enhanced expression of the CCL20 chemokine, the ligand of CCR6, was observed in cancer tissue compared to the normal condition, along with an increased CCL20 gradient in mouse tumor-draining LNs. We proved that TNF-α released by activated-MCs was required to sustain CCL20 production from cancer cells <jats:italic>in vitro</jats:italic> . </jats:p> </jats:sec> <jats:sec> <jats:title>Discussion</jats:title> <jats:p> The accumulation of CCR6 <jats:sup>+</jats:sup> B cells in CRC context may then rely on the crosstalk between MCs and CRC cells. Our findings suggest that B cell immunosurveillance may be indirectly promoted through the clinical modulation of TNF-α secretion at the early stages of colorectal tumorigenesis. </jats:p> </jats:sec>