Abstract
Lung cancer is the leading cause of cancer-associated deaths worldwide, with non-small cell-lung cancer (NSCLC) accounting for approximately 80% of cases. Immune escape has been demonstrated to play a key role in the initiation and progression of NSCLC, although the underlying mechanisms are diverse and their puzzling nature is far from being understood. As a critical participant in immune escape, the CD4+ T cell subset of regulatory T (Treg) cells, with their immunosuppressive functions, has been implicated in the occurrence of many types of cancers. Additionally, therapies based on Treg blockade have benefited a portion of cancer patients, including those with NSCLC. Accumulating literature has noted high Treg infiltration in NSCLC tumor tissues, bone marrow, lymph nodes and/or blood; moreover, the tumor milieu is involved in regulating the proliferation, differentiation, recruitment and suppressive functions of Treg cells. Multifarious mechanisms by which CD4+ Treg cells are generated, attracted and modulated in the NSCLC milieu will be discussed in this review.
Highlights
Lung cancer is continuously evaluated and is considered the leading cause of cancer-related mortality worldwide, with a dismal 5-year survival rate of approximately 19% in the United States [1, 2]
Mechanisms of CD4+ Tregs in nonsmall cell-lung cancer (NSCLC) Progression achieved an unexpected breakthrough in some patients, including those suffering from NSCLC [12,13,14], implying the non-redundant role of immunosuppression in modulating tumor biology
Accumulating evidence suggests that cytokines or other agents derived from NSCLC tissues, as well as phenotype modulators, might be the key factors leading to the differentiation, trafficking and immunosuppressive effects of Tregs
Summary
Lung cancer is continuously evaluated and is considered the leading cause of cancer-related mortality worldwide, with a dismal 5-year survival rate of approximately 19% in the United States [1, 2]. Mechanisms of CD4+ Tregs in NSCLC Progression achieved an unexpected breakthrough in some patients, including those suffering from NSCLC [12,13,14], implying the non-redundant role of immunosuppression in modulating tumor biology. CD4+ regulatory T (Treg) cells, which express the X chromosome-linked, linage specific transcription factor Foxp, are potent immunosuppressive cells and can serve as brakes during immune responses. Treg cells play an opposite role in cancer immunity as Treg cells recruited in tumor tissues become accomplices that help cancer cells escape from immunological surveillance. Accumulating evidence suggests that cytokines or other agents derived from NSCLC tissues, as well as phenotype modulators, might be the key factors leading to the differentiation, trafficking and immunosuppressive effects of Tregs. Of this review, we will discuss the underlying mechanisms in detail
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