抑制树突状细胞中的多巴胺受体D3信号传导可增强抗原向CD8 T细胞的交叉呈递，从而促进抗肿瘤免疫。
Inhibition of dopamine receptor D3 signaling in dendritic cells increases antigen cross-presentation to CD8 T-cells favoring anti-tumor immunity.
作者信息
Figueroa Claudio, Gálvez-Cancino Felipe, Oyarce Cesar, Contreras Francisco, Prado Carolina, Valeria Catalina, Cruz Sebastián, Lladser Alvaro, Pacheco Rodrigo
机构信息
Laboratorio de Neuroinmunología, Fundación Ciencia & Vida, Ñuñoa, 7780272 Santiago, Chile; Departamento de Ciencias Biológicas y Químicas, Facultad de Ciencia, Universidad San Sebastián, Providencia, 7510157 Santiago, Chile.
Laboratorio de Inmunoterapia Génica, Fundación Ciencia & Vida, Ñuñoa, 7780272 Santiago, Chile; Departamento de Ciencias Biológicas, Facultad de Ciencias Biológicas, Universidad Andres Bello, 8370146 Santiago, Chile.
出版信息
J Neuroimmunol. 2017 Feb 15;303:99-107. doi: 10.1016/j.jneuroim.2016.12.014. Epub 2017 Jan 2.
Dendritic cells (DCs) display the unique ability for cross-presenting antigens to CD8 T-cells, promoting their differentiation into cytotoxic T-lymphocytes (CTLs), which play a pivotal role in anti-tumor immunity. Emerging evidence points to dopamine receptor D3 (D3R) as a key regulator of immunity. Accordingly, we studied how D3R regulates DCs function in anti-tumor immunity. The results show that D3R-deficiency in DCs enhanced expansion of CTLs in vivo and induced stronger anti-tumor immunity. Co-culture experiments indicated that D3R-inhibition in DCs potentiated antigen cross-presentation and CTLs activation. Our findings suggest that D3R in DCs constitutes a new therapeutic target to strengthen anti-tumor immunity.
树突状细胞（DCs）具有将抗原交叉呈递给CD8 T细胞的独特能力，促进其分化为细胞毒性T淋巴细胞（CTLs），而CTLs在抗肿瘤免疫中发挥着关键作用。新出现的证据表明多巴胺受体D3（D3R）是免疫的关键调节因子。因此，我们研究了D3R如何调节DCs在抗肿瘤免疫中的功能。结果表明，DCs中D3R的缺失增强了体内CTLs的扩增，并诱导了更强的抗肿瘤免疫。共培养实验表明，DCs中D3R的抑制增强了抗原交叉呈递和CTLs的激活。我们的研究结果表明，DCs中的D3R构成了增强抗肿瘤免疫的新治疗靶点。
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