title: CD20+ B cell depletion in systemic autoimmune diseases: common mechanism of inhibition or disease-specific effect on humoral immunity?
abstract: Autoimmunity remains a complex physiologic deviation, enabled and perpetuated by a variety of interplayers and pathways. Simplistic approaches, targeting either isolated end-effectors of more centrally placed interactors of these mechanisms, are continuously tried in an effort to comprehend and halt cascades with potential disabling and deleterious effects in the affected individuals. This review focuses on theoretical and clinically proved effects of rituximab-induced CD20+ B cell depletion on different systemic autoimmune diseases and extrapolates on pathogenetic mechanisms that may account for different interindividual or interdisease responses.
authors.affiliation: Department of Renal Medicine, Papageorgiou Hospital, 56403 Thessaloniki, Greece.
authors.forename: Panagiotis
authors.initials: P
authors.lastname: Pateinakis
authors.affiliation: 2nd Prop Department of Internal Medicine, Hippokration General Hospital, Konstantinoupoleos 49, 54642 Thessaloniki, Greece.
authors.forename: Athina
authors.initials: A
authors.lastname: Pyrpasopoulou
mesh_terms: D000818:Animals; D058846:Antibodies, Monoclonal, Murine-Derived; D018951:Antigens, CD20; D001327:Autoimmune Diseases; D015551:Autoimmunity; D001402:B-Lymphocytes; D006801:Humans; D056724:Immunity, Humoral; D007155:Immunologic Factors; D051379:Mice; D000069283:Rituximab
chemical_list: D058846:Antibodies, Monoclonal, Murine-Derived; D018951:Antigens, CD20; D007155:Immunologic Factors; D000069283:Rituximab