Specifically, CD3 engagement can stabilize Foxp3 expression and upregulate inhibitory cytokines such as TGF-β, fostering a tolerogenic microenvironment conducive to persistent HPV infection and cervical dysplasia.[18] In addition, HSIL may involve localized CD39 upregulation in the cervical epithelium, driven by chronic inflammation or HPV oncoprotein E6/E7-mediated metabolic reprogramming.[19,20]. Here, TGFB1 is linked to cervical intraepithelial neoplasia.