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Programmed cell death 5 transgenic mice attenuates adjuvant induced arthritis by 2 modifying the T lymphocytes
Feng Yuan1, Junfeng Wang2, Keshi Zhang1
1Arthritis Clinic & Research Center, Peking University People's Hospital, 11 Xizhimen South Street, Xicheng District, Beijing, 100044, China.
Background:
Programmed cell death 5 (PDCD5) is an apoptosis-related gene cloned from TF-1 cells whose primary biological functions are to promote apoptosis and immune regulation. The effects and mechanisms exerted by key mediators of arthritic inflammation remain unclear in PDCD5 transgenic (PDCD5 tg) mice.
Results:
In the current study, PDCD5 tg mice inhibited the progression of adjuvant-induced arthritis, specifically decreasing clinical signs and histological damage, compared with arthritis control mice. Additionally, the ratio of CD4+IFN-γ+ cells (Th1) and CD4+IL-17A+ cells (Th17), as well as the mRNA expression of the pro-inflammatory mediators IFN-γ, IL-6, IL-17A and TNF-α, were decreased in PDCD5 tg mice, while CD4+CD25+Foxp3+ regulatory T (Treg) cells and the anti-inflammatory mediators IL-4 and IL-10 were increased. Furthermore, PDCD5 tg mice demonstrated reduced serum levels of IFN-γ, IL-6, IL-17A and TNF-α and increased levels of IL-4.
Conclusions:
Based on our data, PDCD5 exerts anti-inflammatory effects by modifying the T lymphocytes balance, inhibiting the production of pro-inflammatory mediators and promoting the secretion of anti-inflammatory cytokines, validating PDCD5 protein as a possible treatment for RA.
Insights
Programmed cell death 5 (PDCD5) in transgenic mice reduces arthritis by decreasing inflammatory T cells and increasing regulatory T cells. This suggests PDCD5 protein may be a potential treatment for rheumatoid arthritis (RA).
Area of Science:
- Immunology
- Molecular Biology
- Rheumatology
Background:
- Programmed cell death 5 (PDCD5) is an apoptosis-related gene involved in immune regulation.
- Its role in arthritic inflammation mechanisms in PDCD5 transgenic (PDCD5 tg) mice was previously unclear.
Purpose of the Study:
- To investigate the effects of PDCD5 on the progression and underlying mechanisms of adjuvant-induced arthritis in PDCD5 tg mice.
Main Methods:
- Adjuvant-induced arthritis model in PDCD5 tg mice and control mice.
- Assessment of clinical signs and histological damage.
- Flow cytometry to analyze T cell populations (Th1, Th17, Treg).
- Quantitative PCR for pro-inflammatory (IFN-γ, IL-6, IL-17A, TNF-α) and anti-inflammatory (IL-4, IL-10) cytokine mRNA expression.
- Serum cytokine level analysis.
Main Results:
- PDCD5 tg mice showed inhibited arthritis progression, with reduced clinical and histological damage compared to controls.
- A decrease in pro-inflammatory CD4+IFN-γ+ (Th1) and CD4+IL-17A+ (Th17) cells and their associated cytokines (IFN-γ, IL-6, IL-17A, TNF-α) was observed.
- An increase in regulatory T cells (CD4+CD25+Foxp3+) and anti-inflammatory cytokines (IL-4, IL-10) was noted in PDCD5 tg mice.
Conclusions:
- PDCD5 demonstrates significant anti-inflammatory effects in arthritis.
- It modulates T lymphocyte balance, suppresses pro-inflammatory mediators, and enhances anti-inflammatory cytokines.
- PDCD5 protein is validated as a potential therapeutic target for rheumatoid arthritis (RA).
