title: Depletion of CD4+CD25+Foxp3+ regulatory T cells with anti-CD25 antibody may exacerbate the 1,3-β-glucan-induced lung inflammatory response in mice.
abstract: 1,3-β-Glucan was a major cell wall component of fungus. The existing studies showed that 1,3-β-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-β-glucan-induced lung inflammation is still unclear. In our study, mice were exposed to 1,3-β-glucan by intratracheal instillation. To investigate the role of Treg cells in response to 1,3-β-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-β-glucan-induced lung inflammation. Depletion of Treg cells aggravated the 1,3-β-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-β-glucan-induced lung inflammation.
authors.affiliation: Division of Pneumoconiosis, School of Public Health, China Medical University, 110001, Shenyang, Liaoning, People's Republic of China. aliceliu299@gmail.com
authors.forename: Fangwei
authors.initials: F
authors.lastname: Liu
authors.forename: Dong
authors.initials: D
authors.lastname: Weng
authors.forename: Ying
authors.initials: Y
authors.lastname: Chen
authors.forename: Laiyu
authors.initials: L
authors.lastname: Song
authors.forename: Cuiying
authors.initials: C
authors.lastname: Li
authors.forename: Lei
authors.initials: L
authors.lastname: Dong
authors.forename: Yuan
authors.initials: Y
authors.lastname: Wang
authors.forename: Shasha
authors.initials: S
authors.lastname: Tao
authors.forename: Jie
authors.initials: J
authors.lastname: Chen
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology* / Q000378:metabolism; D018893:Bronchoalveolar Lavage; D016207:Cytokines; D005260:Female; D051858:Forkhead Transcription Factors / Q000276:immunology* / Q000378:metabolism; D066298:In Vitro Techniques; D007249:Inflammation / Q000473:pathology; D053645:Interleukin-2 Receptor alpha Subunit / Q000276:immunology / Q000378:metabolism; D008168:Lung / Q000473:pathology*; D055370:Lung Injury / Q000139:chemically induced / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000378:metabolism; D058408:Th1-Th2 Balance; D047071:beta-Glucans / Q000633:toxicity*
chemical_list: D000911:Antibodies, Monoclonal; D016207:Cytokines; D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; D053645:Interleukin-2 Receptor alpha Subunit; D047071:beta-Glucans; C033363:beta-1,3-glucan