期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 21, 期 17, 页码 -出版社
MDPI
DOI: 10.3390/ijms21176162
关键词
autoimmune arthritis; Nkx2-3; B cell activation
资金
- European Union
- European Social Fund: Project Comprehensive Development for Implementing Smart Specialization Strategies at the University of Pecs [EFOP-3.6.1.-16-2016-00004]
- Janos Bolyai Research Scholarship of The Hungarian Academy of Sciences [BO/00501/19/5]
- New National Excellence Program of the Ministry for Innovation and Technology [UNKP-19-4-P-PTE-458]
- European Social Fund: Project PEPSYS-Complexity of peptide-signalization and its role in systemic diseases [GINOP 2.3.2-15-2016-00050]
- [EFOP-3.6.1-16-2016-00004]
- [GINOP-2.3.2.-15-2016-00048]
B cells play a crucial role in the pathogenesis of rheumatoid arthritis. In Nkx2-3-deficient mice (Nkx2-3(-/-)) the spleen's histological structure is fundamentally changed; therefore, B cell homeostasis is seriously disturbed. Based on this, we were curious, whether autoimmune arthritis could be induced in Nkx2-3(-/-)mice and how B cell activation and function were affected. We induced arthritis with immunization of recombinant human proteoglycan aggrecan G1 domain in Nkx2-3(-/-)and control BALB/c mice. We followed the clinical picture, characterized the radiological changes, the immune response, and intracellular Ca(2+)signaling of B cells. Incidence of the autoimmune arthritis was lower, and the disease severity was milder in Nkx2-3(-/-)mice than in control BALB/c mice. The radiological changes were in line with the clinical picture. In Nkx2-3(-/-)mice, we measured decreased antigen-induced proliferation and cytokine production in spleen cell cultures; in the sera, we found less anti-CCP-IgG2a, IL-17 and IFN gamma, but more IL-1 beta, IL-4 and IL-6. B cells isolated from the lymph nodes of Nkx2-3(-/-)mice showed decreased intracellular Ca(2+)signaling compared to those isolated from BALB/c mice. Our findings show that the transcription factor Nkx2-3 might regulate the development of autoimmune arthritis most likely through modifying B cell activation.
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