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Multiple endogenous antigens refers to the collective set of self-molecules, including cytokines, cell surface receptors, and circulating proteins, that are modulated by broad-spectrum polyclonal therapies (Kazatchkine & Kaveri, 2001). This term is most frequently utilized in pharmacological contexts to describe the target profile of Intravenous Immunoglobulin (IVIG), which contains a vast array of naturally occurring antibodies derived from large plasma pools (Galeotti et al., 2017). These antibodies function by neutralizing pathogenic autoantibodies, interfering with the complement cascade, and saturating Fc receptors on immune cells to dampen systemic inflammation (Jolles et al., 2005). Because the therapy interacts with a wide variety of host proteins to restore immune homeostasis, it is categorized under this aggregate heading rather than a single molecular entity. This multi-target approach is particularly effective in treating multifaceted autoimmune disorders like Kawasaki disease and Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) where multiple pathways are dysregulated (Lünemann et al., 2015). The interaction with these antigens allows for the modulation of B-cell and T-cell activation, as well as the neutralization of superantigens (Kaveri et al., 2011).
The mechanism involves the neutralization of circulating autoantibodies and inflammatory cytokines, competitive inhibition of Fc receptors on phagocytic cells, and the modulation of complement-mediated damage (Galeotti et al., 2017; Kazatchkine & Kaveri, 2001).
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