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CD5-positive regulatory B cells (Bregs), often referred to as B10 cells, are a specialized subset of B lymphocytes characterized by their ability to suppress immune responses, primarily through the secretion of interleukin-10 (IL-10) [1, 6]. These cells play a crucial role in maintaining peripheral tolerance and preventing autoimmunity by inhibiting the activation and expansion of pro-inflammatory T cells and other immune effectors [1, 5]. In the context of disease, a deficiency or dysfunction of CD5+ Bregs is associated with various autoimmune conditions, such as systemic lupus erythematosus and rheumatoid arthritis, where their loss leads to uncontrolled inflammation [4, 11]. Conversely, in cancer, these cells can be recruited to the tumor microenvironment where they promote immune evasion and tumor growth by dampening anti-tumor immunity [5, 8]. Therapeutic strategies involving CD5+ Bregs include their depletion in B-cell malignancies or their induction and expansion to treat autoimmune diseases and graft-versus-host disease [2, 9, 10]. CD5 itself is a transmembrane glycoprotein that acts as a negative regulator of B-cell receptor (BCR) signaling, further contributing to the anergic and regulatory phenotype of these cells [3, 6].
B-cell depletion via antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC); inhibition of B-cell survival and activation; induction of regulatory B-cell expansion and IL-10 production; targeted cytotoxicity against CD5-expressing cells.
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