Version 1
: Received: 1 May 2024 / Approved: 2 May 2024 / Online: 2 May 2024 (08:08:13 CEST)
How to cite:
Mirzaesmaeili, A.; Abdul-Sater, A. A. TRAF1 Deficiency in Macrophages Drives Exacerbated Joint Inflammation in Rheumatoid Arthritis. Preprints2024, 2024050107. https://doi.org/10.20944/preprints202405.0107.v1
Mirzaesmaeili, A.; Abdul-Sater, A. A. TRAF1 Deficiency in Macrophages Drives Exacerbated Joint Inflammation in Rheumatoid Arthritis. Preprints 2024, 2024050107. https://doi.org/10.20944/preprints202405.0107.v1
Mirzaesmaeili, A.; Abdul-Sater, A. A. TRAF1 Deficiency in Macrophages Drives Exacerbated Joint Inflammation in Rheumatoid Arthritis. Preprints2024, 2024050107. https://doi.org/10.20944/preprints202405.0107.v1
APA Style
Mirzaesmaeili, A., & Abdul-Sater, A. A. (2024). TRAF1 Deficiency in Macrophages Drives Exacerbated Joint Inflammation in Rheumatoid Arthritis. Preprints. https://doi.org/10.20944/preprints202405.0107.v1
Chicago/Turabian Style
Mirzaesmaeili, A. and Ali A. Abdul-Sater. 2024 "TRAF1 Deficiency in Macrophages Drives Exacerbated Joint Inflammation in Rheumatoid Arthritis" Preprints. https://doi.org/10.20944/preprints202405.0107.v1
Abstract
The tumor necrosis factor receptor associated factor 1 (TRAF1) plays a key role in promoting lymphocyte survival, proliferation, and cytokine production. Recent evidence showed that TRAF1 plays opposing roles in monocytes and macrophages where it controls NF-B activation and limits pro-inflammatory cytokine production as well as inflammasome-dependent IL-1 secretion. Importantly, TRAF1 polymorphisms have been strongly linked to an increased risk of rheumatoid arthritis (RA). However, whether and how TRAF1 contributes to RA pathogenesis is not fully understood. Moreover, investigating the role of TRAF1 in driving RA pathogenesis is complicated by its multifaceted and opposing roles in various immune cells. In this study, we show that intraarticular injection of TRAF1 deficient macrophages into knee joints of wildtype (WT) mice subjected to the collagen antibody induced arthritis (CAIA) model of RA significantly exacerbated joint inflammation, immune cell infiltration and tissue damage compared to mice injected with WT macrophages. This study may lay the groundwork for novel therapies for RA that target TRAF1 in macrophages.
Biology and Life Sciences, Immunology and Microbiology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
