Figure 3.
Proposed mechanism of vital TET formation in acne. In the pilosebaceous follicles, C. acnes strains trigger antigen presenting cells to secrete cytokines that induce naïve T cells to differentiate into distinct T cell subsets. Upon induction, AMTH17 cells can further be activated by bacterial ligands, PMA and other stimuli. TCR-ligand binding induce the formation of vesicles containing DNA. Blebbing of T cell nuclear envelope, vesicular exportation and exocytosis of vesicles containing DNA generate extracellular traps while preserving the integrity of the cell. As a result, AMTH17 cells retain conventional functions of viable T cells such as cytokine secretion. In vitro, we have observed that AMTH17 cells release TETs as early as 30 minutes after stimulation with C. acnes. Both the released TETs and IL-17 can recruit neutrophils to inflamed acne lesions. TETs trap C. acnes and are also loaded with antimicrobial molecules, including granulysin and histone H2B, H3 and H4 that kill bacteria. Created with BioRender.com.