ABSTRACT
The loss of tolerance to self-antigens is the unequivocal “red line” of autoimmunity: both development of autoreactive T and B cells and production of polyclonal autoantibodies represent seminal keys to the pathogenesis of protean autoimmune diseases. Most of these autoantibodies are immunoglobulins G (IgG), functionally distinguished in four subclasses named IgG1, IgG2, IgG3, and IgG4, due to structural differences in the hinge and heavy chain constant regions. Different studies analyzed serum levels of IgG subclasses in the course of different disorders, showing that they might have a pathogenic role by regulating interactions among immunoglobulins, Fc-gamma receptors, and complement. To date, the mechanisms promoting different IgG subclasses distribution during the natural history of most autoimmune diseases remain somewhat unclear. Evidence from the medical literature shows that the serum IgG profile is peculiar for many autoimmune diseases, suggesting that different subclasses could be specific for the underlying driving autoantigens. A better knowledge of IgG subsets may probably help to elucidate their pathological task, but also to define their relevance for diagnostic purposes, patients’ personalized management, and prognosis assessment.
Acknowledgments
This review and its publication have been supported from Università Cattolica del Sacro Cuore Fondazione Policlinico Universitario Agostino Gemelli IRCCS as a part of its programs on promotion and dissemination of scientific research (Linea D1 to MM), that we gratefully acknowledged.
This research did not receive any grant from funding agencies involved in any public, commercial, or no-profit sectors.
Declaration of interest statement
The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Correction Statement
This article has been republished with minor changes. These changes do not impact the academic content of the article.