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Abstract
MHCI molecules present antigens to CD8⁺ T cells, but mechanisms of antigen processing for non-classically restricted T cells remain poorly understood. This study identifies Rab6 as essential for presenting Mycobacterium tuberculosis antigens to MR1-restricted T cells in infected epithelial cells, but not for classical MHCI or HLA-E pathways. Rab6 knockdown and imaging revealed that Rab6 does not affect MR1 surface expression or ligand-induced translocation, suggesting its role is unrelated to MR1 trafficking. These findings implicate Rab6 in antigen processing rather than MR1 transport, providing a basis for future studies on intracellular trafficking in MR1-mediated immunity.