A tunnel microtract (TMT) organ derived from neural crest cells serves as a dedicated conduit for T cell progenitor homing to the thymus in both zebrafish and mice, with Sox10 directly activating Cdc42 to drive F-actin reorganization that controls the morphogenetic transition of neural crest cells from rounded to spindle-shaped epithelial cells, thereby establishing a low-permeability barrier essential for directional T cell progenitor trafficking and pre-thymic lineage priming.

Thymic colonization by T cell progenitors (TCPs) is essential for adaptive immunity, yet the guiding tissues remain elusive. Here, we unveiled a tunnel microtract (TMT) as an organ indispensable in TCPs homing in both zebrafish and mouse. Disruption of TMT leads to compromised T cell development. Specifically, the zebrafish TMT were positioned bilaterally beneath the fifth branchial levator muscle, connecting the thymus and kidney. They are semi-coiled, non-vascular, non-lymphatic tubes of epithelial signatures. Impressively, Sox10 activates Cdc42 to promote F-actin remodeling in neural crest cells (NCCs), leading to precise elongation and tight packaging of a low-permeability TMT. Remarkably, a homologous CD34⁺ TMT was observed in mice, which bilaterally enveloped the embryonic thymus and extended into the thyroid cartilage. Sox10-Cdc42 signalling functioned recapitulatively in NCC morphogenesis during its construction. These findings establish TMT as an unappreciated NCC-derived organ in TCPs homing, with implications in T cell development and immune disorders.