优爱(UA BIOSCIENCE)-重组蛋白专家

Accumulation of regulatory T (Treg) cells, an immunosuppressive population, limits the efficacy of immunotherapy in NSCLC. C-C motif chemokine receptor 8 (CCR8) is selectively expressed in tumor-infiltrating Treg cells and is, therefore, considered an ideal target.

Sepsis, a leading cause of mortality in intensive care units worldwide, lacks effective treatments for advanced-stage sepsis. Therefore, understanding the underlying mechanisms of this disease is crucial. This studyreveals that invariant natural killer T (iNKT) cells have an opposing role in the progression of sepsis by suppressing regulatory T (Treg) cell differentiation and function. The activation of iNKT cells by a-Galcer enhances interferon (IFN)-g production. Blocking antibodies or transferring IFN-g-deficient iNKT cells dem onstrates that iNKT cells inhibit Treg differentiation through IFN-g production. Additionally, iNKT cell-medi ated Treg inhibition prevents secondary infection caused by Listeria monocytogenes during the post-septic phase. The transcriptomic analysis of Treg cells further reveals that the suppressive function of Tregs is impaired byiNKTcells.Finally, we demonstratethat iNKT cells inhibit Treg differentiation in an Nr4a1-depen dent manner. Our data uncover the dual function of iNKT cells in sepsis progression and provide a potential treatment target for this adverse long-term outcome induced by sepsis