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The role of regulatory T cells in the pathogenesis and treatment of prostate cancer

前列腺癌 医学 免疫疗法 FOXP3型 癌症 免疫系统 前列腺 癌症研究 免疫学 转移 抗原 免疫耐受 肿瘤进展 肿瘤科 内科学
作者
Vahid Karpisheh,Seyedeh Mahboubeh Mousavi,Parinaz Naghavi Sheykholeslami,Mehrdad Fathi,Mehran Mohammadpour Saray,Leili Aghebati‐Maleki,Reza Jafari,Naime Majidi Zolbanin,Farhad Jadidi‐Niaragh
出处
期刊:Life Sciences [Elsevier]
卷期号:284: 119132-119132 被引量:46
标识
DOI:10.1016/j.lfs.2021.119132
摘要

Despite developments in the treatment of various cancers, prostate cancer is one of the deadliest diseases known to men. Systemic therapies such as androgen deprivation, chemotherapy, and radiation therapy have not been very successful in treating this disease. Numerous studies have shown that there is a direct relationship between cancer progression and inhibition of anti-tumor immune responses that can lead to progression of various malignancies, including prostate cancer. Interestingly, CD4+CD25+FoxP3+ regulatory T cells significantly accumulate and increase in draining lymph nodes and PBMCs of patients with prostate cancer and other solid tumors. In vivo and in vitro studies have shown that Tregs can suppress anti-tumor responses, which is directly related to the increased risk of cancer recurrence. Tregs are essential for preserving self-tolerance and inhibiting extra immune responses harmful to the host. Since the tumor-related antigens are mainly self-antigens, Tregs could play a major role in tumor progression. Accordingly, it has discovered that prostate cancer patients with higher Tregs have poor prognosis and low survival rates. However, anti-tumor responses can be reinforced by suppression of Tregs with using monoclonal antibodies against CD25 and CTLA-4. Therefore, depleting Tregs or suppressing their functions could be one of the effective ways for prostate cancer immunotherapy. The purpose of this review is to investigate the role of Treg cells in the progression of prostate cancer and to evaluate effective strategies for the treatment of prostate cancer by regulating Treg cells.
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