Expression of Hv1 proton channels in myeloid-derived suppressor cells (MDSC) and its potential role in T cell regulation

Author:

Alvear-Arias Juan J.12ORCID,Carrillo Christian12ORCID,Villar Javiera Paz1ORCID,Garcia-Betancourt Richard1,Peña-Pichicoi Antonio12,Fernandez Audry1,Fernandez Miguel12,Carmona Emerson M.1ORCID,Pupo Amaury1,Neely Alan1ORCID,Alvarez Osvaldo13ORCID,Garate Jose12ORCID,Barajas-Martinez Héctor4ORCID,Larsson H. Peter5ORCID,Lopez-Rodriguez Angélica6ORCID,Latorre Ramon1ORCID,Gonzalez Carlos123

Affiliation:

1. Millenium Institute Centro Interdisciplinario de Neurociencia de Valparaíso, Facultad de Ciencias, Universidad de Valparaíso, Valparaíso 236 0102, Chile

2. Millenium Nucleus in NanoBioPhysics (NNBP), Universidad de Valparaíso, Valparaíso 236 0102, Chile

3. Departamento de Biología, Facultad de Ciencias, Universidad de Chile, Santiago 7800003, Chile

4. Cardiovascular Research, Lankenau Institute for Medical Research, Wynnewood, PA 19096

5. Department of Physiology & Biophysics, University of Miami, Coral Gables, FL 33101

6. Facultad de Ciencias Químicas, Universidad Juárez del Estado de Durango, Durango 34000, México

Abstract

SignificanceImmunosuppression by myeloid-derived suppressor cells (MDSC), especially near tumor surfaces, involves the extracellular production of reactive oxygen species (ROS). ROS generation in MDSC occurs during the oxidation of NADPH to NADP+, which NOX2 catalyzes. ROS react with the T cell receptor complex, abolishing the antigen presentation, which blocks the immune system elimination of the tumor cells. Extrusion of protons from MDSC by voltage-gated proton channel (Hv1) sustains ROS production. Here, we demonstrate the expression of Hv1 in mouse MDSC. In this way, Hv1 present in MDSC becomes a potential cancer therapeutic target since its inhibition seems to diminish immunosuppression activity in the tumoral microenvironment, allowing cancer cells to be attacked by the immune system.

Publisher

Proceedings of the National Academy of Sciences

Subject

Multidisciplinary

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3