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Regulatory T cells (Tregs) and regulatory B cells (Bregs) are specialized lymphocyte subpopulations that maintain immune homeostasis and self-tolerance by suppressing excessive immune responses (Sakaguchi et al., 1995; Mauri & Bosma, 2012). Tregs are characterized by the expression of the transcription factor FOXP3 and the CD25 surface marker, while Bregs are primarily identified by their secretion of the anti-inflammatory cytokine IL-10 (Vignali et al., 2008; Rosser & Mauri, 2015). In oncology, these cells often accumulate within the tumor microenvironment, where they inhibit anti-tumor effector cells and promote immune evasion (Selby et al., 2013). Conversely, their deficiency or dysfunction is linked to the pathogenesis of autoimmune diseases and chronic inflammatory conditions (Klatzmann & Abbas, 2015). Therapeutic interventions aim to either deplete these cells to enhance immunity in cancer or expand them to restore tolerance in autoimmunity and transplantation (Klatzmann & Abbas, 2015; Mahne et al., 2015). Common pharmacological agents include low-dose IL-2 for Treg expansion and monoclonal antibodies like ipilimumab or mogamulizumab for Treg depletion (Selby et al., 2013; Mahne et al., 2015).
Regulatory cell depletion, regulatory cell expansion, and immune checkpoint modulation
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