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Endophilin A2 deficiency protects rodents from autoimmune arthritis by modulating T cell activation
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Endophilin A2 deficiency protects rodents from autoimmune arthritis by modulating T cell activation
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Journal Article
Endophilin A2 deficiency protects rodents from autoimmune arthritis by modulating T cell activation
2021
Overview
The introduction of the CTLA-4 recombinant fusion protein has demonstrated therapeutic effects by selectively modulating T-cell activation in rheumatoid arthritis. Here we show, using a forward genetic approach, that a mutation in the
SH3gl1
gene encoding the endocytic protein Endophilin A2 is associated with the development of arthritis in rodents. Defective expression of
SH3gl1
affects T cell effector functions and alters the activation threshold of autoreactive T cells, thereby leading to complete protection from chronic autoimmune inflammatory disease in both mice and rats. We further show that
SH3GL1
regulates human T cell signaling and T cell receptor internalization, and its expression is upregulated in rheumatoid arthritis patients. Collectively our data identify SH3GL1 as a key regulator of T cell activation, and as a potential target for treatment of autoimmune diseases.
The autoimmune disorder, rheumatoid arthritis (RA), has been associated with multiple pathophysiological factors. Here the authors show that deficiency in endophilin A2 in rodents protects them from experimental arthritis by altering T cell activation threshold and effector functions, thereby hinting a potential target for RA therapy.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/1
/ 13/21
/ 13/31
/ 38/15
/ 38/23
/ 38/77
/ 45/90
/ 45/91
/ 64/60
/ Acyltransferases - deficiency
/ Acyltransferases - metabolism
/ Animals
/ Arthritis, Rheumatoid - enzymology
/ Arthritis, Rheumatoid - immunology
/ Arthritis, Rheumatoid - prevention & control
/ Autoimmune Diseases - enzymology
/ Autoimmune Diseases - immunology
/ Autoimmunitet och inflammation
/ Autoimmunity and Inflammation
/ Female
/ Humanities and Social Sciences
/ Humans
/ Kinases
/ Lymphocyte Activation - immunology
/ Male
/ Mice
/ Mutation
/ Proteins
/ Rats
/ Receptors, Antigen, T-Cell - metabolism
/ Rodents
/ Science
