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组织蛋白酶S调节非霍奇金淋巴瘤的抗原加工和T细胞活性
作者:小柯机器人 发布时间:2020/4/26 13:33:05

瑞士联邦理工学院Elisa Oricchio小组的最新研究发现,组织蛋白酶S调节非霍奇金淋巴瘤的抗原加工和T细胞活性。这一研究成果于2020年4月23日在线发表在《癌细胞》上。

研究人员发现,滤泡性淋巴瘤患者在组织蛋白酶S(CTSS)中具有针对酪氨酸132(Y132D)的复发性热点突变,可增强蛋白质活性。CTSS调节抗原加工以及CD4+和CD8+T细胞介导的免疫反应。CTSS活性的丧失会通过限制与CD4+滤泡性辅助T细胞的交流来减少淋巴瘤的生长,同时诱导抗原多样化和CD8+T细胞的活化。
 
总的来说,这些结果表明CTSS抑制具有非冗余的治疗潜力,可以增强惰性和侵袭性淋巴瘤的抗肿瘤免疫反应。
 
据了解,癌细胞中的基因组改变会影响免疫系统,从而促进肿瘤生长。在非霍奇金淋巴瘤中,B细胞与生发中心微环境之间的生理相互作用被认为可以维持癌细胞的增殖。
 
附:英文原文

Title: Cathepsin S Regulates Antigen Processing and T Cell Activity in Non-Hodgkin Lymphoma

Author: Elie Dheilly, Elena Battistello, Natalya Katanayeva, Stephanie Sungalee, Justine Michaux, Gerben Duns, Sarah Wehrle, Jessica Sordet-Dessimoz, Marco Mina, Julien Racle, Pedro Farinha, George Coukos, David Gfeller, Anja Mottok, Robert Kridel, Bruno E. Correia, Christian Steidl, Michal Bassani-Sternberg, Giovanni Ciriello, Vincent Zoete, Elisa Oricchio

Issue&Volume: 2020-04-23

Abstract: Genomic alterations in cancer cells can influence the immune system to favor tumorgrowth. In non-Hodgkin lymphoma, physiological interactions between B cells and thegerminal center microenvironment are coopted to sustain cancer cell proliferation.We found that follicular lymphoma patients harbor a recurrent hotspot mutation targetingtyrosine 132 (Y132D) in cathepsin S (CTSS) that enhances protein activity. CTSS regulatesantigen processing and CD4+ and CD8+ T cell-mediated immune responses. Loss of CTSS activity reduces lymphoma growth bylimiting communication with CD4+ T follicular helper cells while inducing antigen diversification and activation ofCD8+ T cells. Overall, our results suggest that CTSS inhibition has non-redundant therapeuticpotential to enhance anti-tumor immune responses in indolent and aggressive lymphomas.

DOI: 10.1016/j.ccell.2020.03.016

Source: https://www.cell.com/cancer-cell/fulltext/S1535-6108(20)30156-2

期刊信息

Cancer Cell:《癌细胞》,创刊于2002年。隶属于细胞出版社,最新IF:23.916
官方网址:https://www.cell.com/cancer-cell/home
投稿链接:https://www.editorialmanager.com/cancer-cell/default.aspx