
IL-2 처리는 만성 감염에서 CD8+ T 세포의 효과기 기능을 증가시키지만, CXCR5+ TPEX 세포 형성과 B 세포 여포 내 감염 억제를 저해한다.


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Cytotoxic CD8+ T cells, essential in combating viral infections and cancer, become dysfunctional from prolonged antigen exposure. Precursors of exhausted T (TPEX) cells are pivotal in sustaining immune responses in chronic diseases and mediating immunotherapy efficacy. They also control viral infection within B-cell follicles, facilitated by CXCR5 expression. How cytokines regulate TPEX cell fate and follicular entry is not well understood. We reveal that IL-2 treatment enhances CD8+ T cell effector functions in chronic LCMV infection but hinders CXCR5+ TPEX cell formation and infection control within B-cell follicles. Mechanistically, IL-2 suppresses TPEX cell differentiation in a STAT5 and BLIMP1-dependent manner. Using an IL-2 fusion protein targeting CD122, we shifted the differentiation towards CX3CR1+ T cells with increased effector function. Clinical observations with low-dose IL-2 in autoimmune disease confirmed IL-2’s inhibitory effect on CXCR5+ TPEX cells, underscoring IL-2’s crucial regulatory role and therapeutic potential in modulating TPEX and effector T cell generation.

### Competing Interest Statement

The authors have declared no competing interest.

IL-2 enhances effector function but suppresses follicular localization of CD8+ T cells in chronic infection

만성-감염에서-il-2는-cd8-t-세포의-효과기-기능을-강화하지만-여포-내-국소화를-억제한다


만성 감염에서 IL-2는 CD8+ T 세포의 효과기 기능을 강화하지만 여포 내 국소화를 억제한다
