CD20+ B Cell Depletion in Systemic Autoimmune Diseases: Common Mechanism of Inhibition or Disease-Specific Effect on Humoral Immunity? | Zendy

Panagiotis Pateinakis | Zendy; Athina Pyrpasopoulou | Zendy

Open Access

CD20+ B Cell Depletion in Systemic Autoimmune Diseases: Common Mechanism of Inhibition or Disease-Specific Effect on Humoral Immunity?

Author(s) -

Panagiotis Pateinakis,

Athina Pyrpasopoulou

Publication year - 2014

Publication title -

biomed research international

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.772

H-Index - 126

eISSN - 2314-6141

pISSN - 2314-6133

DOI - 10.1155/2014/973609

Subject(s) - autoimmunity , mechanism (biology) , immunology , rituximab , disease , effector , immunity , autoimmune disease , b cell , medicine , biology , immune system , neuroscience , antibody , philosophy , epistemology

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.

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