Immune checkpoints and the multiple faces of B cells in systemic lupus erythematosus. Issue 6 (November 2021)

• Record Type: Journal Article
• Authors: Stefanski, Ana-Luisa; Dörner, Thomas
• Is Part Of: Current opinion in rheumatology. Volume 33:Issue 6(2021)
• Publication Date: 2021-11
• Subjects: B cells -- CD40 -- checkpoint molecules -- systemic lupus erythematosus; Rheumatology -- Periodicals; Arthritis -- Periodicals; Review Literature -- Periodicals; Rheumatic Diseases -- Periodicals; 616.723
• DOI: 10.1097/BOR.0000000000000825
• Languages: English
• ISSNs: 1040-8711

Abstract

Abstract : Purpose of review: B-lymphocytes are crucial in the pathogenesis of systemic lupus erythematosus (SLE), including autoantibody production, antigen presentation, co-stimulation, and cytokine secretion. Co-stimulatory and co-inhibitory molecules control interactions between B and T cells during an inflammatory response, which is essential for an appropriate host protection and maintenance of self-tolerance. Here, we review recent findings about checkpoint molecules and SLE B cells including their potential therapeutic implications and experiences from clinical trials. Recent findings: Most prominent checkpoint molecules involved in pathologic B and T cell interaction in SLE are CD40/CD40L and inducible co-stimulator/ICOSL, both also intimately involved in the formation of germinal centers and ectopic lymphoid tissue. Dysregulations of inhibitory checkpoint molecules, like programmed death-1/programmed death-ligand 1 and B- and T-lymphocyte attenuator have been suggested to impair B cell functions in SLE recently. Summary: Accumulating evidence indicates that dampening immune responses by either blocking co-activating signals or enhancing co-inhibitory signals in different cell types is a promising approach to treat autoimmune diseases to better control active disease but may also allow resolution of chronic autoimmunity.