Polyclonal immune receptors

Polyclonal immune receptors refer to the vast and diverse collection of antigen-recognition molecules, primarily T-cell receptors (TCRs) and B-cell receptors (BCRs), expressed across the lymphocyte population. These receptors are generated through complex genetic recombination processes, allowing the immune system to identify an almost limitless variety of epitopes from pathogens and abnormal cells (Janeway et al., 2001). In a therapeutic context, these receptors are targeted collectively by polyclonal antibody preparations such as antithymocyte globulin (ATG) or intravenous immunoglobulin (IVIG). ATG works by binding to a broad spectrum of these receptors and other surface markers on T-cells, leading to their depletion and the suppression of cellular immunity (Mohty, 2006). This broad-spectrum approach is particularly effective in preventing acute organ transplant rejection and treating graft-versus-host disease (GVHD). However, because these therapies interact with a wide array of polyclonal receptors rather than a single specific target, they can cause systemic immune activation, such as cytokine release syndrome, or lead to profound, non-selective immunosuppression (StatPearls, 2023).

Other names

Immune receptor repertoirePolyclonal T-cell receptorsPolyclonal B-cell receptorsLymphocyte antigen receptorsPolyclonal T-lymphocyte surface antigens

Polyclonal antibody preparations bind to a wide array of epitopes on various immune receptors (e.g., CD2, CD3, CD4, CD8, TCR), inducing cell depletion through complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC) (Mohty, 2006). Additionally, intravenous immunoglobulin (IVIG) interacts with Fc receptors and neutralizes circulating cytokines and autoantibodies to modulate immune responses (Kazatchkine & Kaveri, 2001).