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Inhibition of dopamine receptor D3 signaling in dendritic cells increases antigen cross-presentation to CD8+ T-cells favoring anti-tumor immunity.

Figueroa C., Gálvez-Cancino F., Oyarce C., Contreras F., Prado C., Valeria C., Cruz S., Lladser A., Pacheco R.

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.

More information Original publication

DOI

10.1016/j.jneuroim.2016.12.014

Type

Journal article

Publication Date

2017-02-01T00:00:00+00:00

Volume

303

Pages

99 - 107

Total pages

8

Addresses

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Keywords

Dendritic Cells, CD8-Positive T-Lymphocytes, Animals, Mice, Inbred C57BL, Mice, Transgenic, Mice, Knockout, Mice, Melanoma, Experimental, Antigens, Neoplasm, Tumor Burden, Signal Transduction, Antigen Presentation, Male, Receptors, Dopamine D3, Mice, 129 Strain