AIM2 regulates anti-tumor immunity and is a viable therapeutic target for melanoma.
AIM2 regulates anti-tumor immunity and is a viable therapeutic target for melanoma.
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DOI:
10.1084/jem.20200962
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发表时间:
2021-09-06
期刊:
影响因子:
--
通讯作者:
Harris JE
中科院分区:
文献类型:
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作者:
Fukuda K;Okamura K;Riding RL;Fan X;Afshari K;Haddadi NS;McCauley SM;Guney MH;Luban J;Funakoshi T;Yaguchi T;Kawakami Y;Khvorova A;Fitzgerald KA;Harris JE
Fukuda et al. demonstrate that AIM2 expression in DCs within human melanoma is a poor prognostic sign and that AIM2-deficient DC vaccination enhances melanoma immunotherapeutic responses by promoting STING-induced IFN secretion as well as limiting IL-1β and IL-18 production. The STING and absent in melanoma 2 (AIM2) pathways are activated by the presence of cytosolic DNA, and STING agonists enhance immunotherapeutic responses. Here, we show that dendritic cell (DC) expression of AIM2 within human melanoma correlates with poor prognosis and, in contrast to STING, AIM2 exerts an immunosuppressive effect within the melanoma microenvironment. Vaccination with AIM2-deficient DCs improves the efficacy of both adoptive T cell therapy and anti–PD-1 immunotherapy for “cold tumors,” which exhibit poor therapeutic responses. This effect did not depend on prolonged survival of vaccinated DCs, but on tumor-derived DNA that activates STING-dependent type I IFN secretion and subsequent production of CXCL10 to recruit CD8+ T cells. Additionally, loss of AIM2-dependent IL-1β and IL-18 processing enhanced the treatment response further by limiting the recruitment of regulatory T cells. Finally, AIM2 siRNA-treated mouse DCs in vivo and human DCs in vitro enhanced similar anti-tumor immune responses. Thus, targeting AIM2 in tumor-infiltrating DCs is a promising new treatment strategy for melanoma.