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Rheumatoid arthritis (RA) is a complex autoimmune disorder characterized by a spectrum of hypersensitivity reactions, encompassing Type II, Type III, and Type IV responses. Firstly, RA is marked by Type II hypersensitivity reactions driven by autoantibodies, such as rheumatoid factor (RF) and anti-(cyclic) citrullinated protein antibodies (ACPAs). These autoantibodies serve not only as serological markers for RA but also actively participate in inflammation, bone erosion, and clinical outcomes, with concurrent activation of the complement system involving C1q, C3, and C5 components specifically linked to RA progression and bone damage. Secondly, RA exhibits traits of Type III hypersensitivity, marked by the formation of immune complexes inciting inflammatory reactions. Immunoglobulin G (IgG) autoantibodies like RF and ACPA play pivotal roles in immune complex formation and the ensuing inflammatory responses. RA also demonstrates Type IV hypersensitivity propelled by CD4+ T cells, encompassing T helper 1 (Th1) and Th17 subsets. Th1 cells release interferon (IFN)-γ, promoting proinflammatory cytokines, while Th17 cells secrete IL-17, IL-22, and granulocyte-macrophage colony-stimulating factor (GM-CSF), contributing to synovial inflammation, bone and cartilage damage, and angiogenesis. RA concurrently exhibits features of Type II, Type III, and Type IV hypersensitivity. It is crucial to comprehend the presence and complex interplay of hypersensitivity responses and specific immune cell subsets in RA to create precise and efficient therapeutic approaches for the management of this incapacitating autoimmune condition. Thus, in this review, we aim to provide a comprehensive overview of the hypersensitivity features of RA.
Heo et al. (Thu,) studied this question.