Depletion of CD4+CD25+Foxp3+regulatory T cells with anti-CD25 antibody may exacerbate the 1,3-beta-glucan-induced lung inflammatory response in mice

作者：Liu Fangwei; Weng Dong; Chen Ying; Song Laiyu; Li Cuiying; Dong Lei; Wang Yuan; Tao Shasha; Chen Jie^*

来源：Archives of Toxicology, 2011, 85(11): 1383-1394.

DOI：10.1007/s00204-011-0673-6

• 1,3-beta-glucan
• Regulatory T cells
• Lung inflammation
• Th1/Th2

1,3-beta-Glucan was a major cell wall component of fungus. The existing studies showed that 1,3-beta-glucan exposure could induce lung inflammation that involved both Th1 and Th2 cytokines. Regulatory T cells (Treg cells) played a critical role in regulating immune homeostasis by adjusting the Th1/Th2 balance. The role of Treg cells and regulatory mechanism in 1,3-beta-glucan-induced lung inflammation is still unclear. In our study, mice were exposed to 1,3-beta-glucan by intratracheal instillation. To investigate the role of Treg cells in response to 1,3-beta-glucan, we generated Treg-depleted mice by intraperitoneal administration of anti-CD25 mAb. The Treg-depleted mice showed more inflammatory cells and severer pathological inflammatory change in lung tissue. Depletion of Treg cells led to increased Th1 cytokines and decreased Th2 cytokines. Treg-depleted mice showed a decreased expression of anti-inflammation cytokine and lower-level expression of CTLA-4. In all, our study indicated that Treg cells participated in regulating the 1,3-beta-glucan-induced lung inflammation. Depletion of Treg cells aggravated the 1,3-beta-glucan-induced lung inflammation, regulated the Th1/Th2 balance by enhancing Th1 response. Treg cells exerted their modulation function depending on both direct and indirect mechanism during the 1,3-beta-glucan-induced lung inflammation.

• 出版日期2011-11
• 单位中国医科大学