Abstract
A large number of cancer patients relapse after chemotherapeutic treatment. The immune system is capable of identifying and destroying cancer cells, so recent studies have highlighted the growing importance of using combinatorial chemotherapy and immunotherapy. However, many patients have innate or acquired resistance to immunotherapies. Long-term follow-up in a pooled meta-analysis exhibited long-term survival in approximately 20% of patients treated with immune checkpoint inhibitors or the adoptive transfer of chimeric T cells. It has been reported that high levels of immunoregulatory cells in cancer patients contribute to immunotherapy resistance via immunosuppression. Among the most important regulatory cell subtypes are the CD4+ T-regulatory cells (Tregs), identified by their expression of the well-characterized, lineage-specific transcription factor FOXP3. In addition to CD4+ Tregs, other regulatory cells present in the tumor microenvironment, namely CD8+ Tregs and IL10-producing B-regulatory cells (Bregs) that also modulate the immune response in solid and lymphoid tumors. These cells together have detrimental effects on tumor immune surveillance and anti-tumor immunity. Therefore, targeting these regulatory lymphocytes will be crucial in improving treatment outcomes for immunotherapy.
Highlights
The suppression of anti-tumor immune responses and augmentation of tumor-promoting immune responses both contribute to tumor progression [1]
Recent research in B-cell biology has found a novel IL10-producing subset of B cells that modulates tumor immune responses. This population has been designated as B-regulatory cells (Bregs), which play a significant role in the harmonization of immune responses involved in autoimmunity, inflammation, and cancer [12]
One study demonstrated that patients with hepatocellular carcinoma contain a higher number of suppressive CD4+CD25+fork-head box-p3 (FOXP3)+ T-regulatory cell (Treg), and depleting this population by blocking surface receptors like cytotoxic T-lymphocyte-associated protein-4 (CTLA4), CD25, or various chemokine receptors could enhance anti-tumor immunity [23, 24]
Summary
The suppression of anti-tumor immune responses and augmentation of tumor-promoting immune responses both contribute to tumor progression [1]. This population has been designated as B-regulatory cells (Bregs), which play a significant role in the harmonization of immune responses involved in autoimmunity, inflammation, and cancer [12]. Bregs generally suppress other cells, including T cells through secretion of the anti-inflammatory cytokine IL10, and they can facilitate the conversion of T-effecter cells into Tregs, attenuating anti-tumor immune responses.
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