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CTLA4-Ig 可调节胶原诱导性关节炎小鼠的树突状细胞，增加 CD4+CD25+Foxp3+ 调节性 T 细胞群体。

CTLA4-Ig modifies dendritic cells from mice with collagen-induced arthritis to increase the CD4+CD25+Foxp3+ regulatory T cell population.

机构信息

Division of Rheumatology, Department of Internal Medicine, The Catholic University of Korea, School of Medicine, Seoul, South Korea.

出版信息

J Autoimmun. 2010 Mar;34(2):111-20. doi: 10.1016/j.jaut.2009.07.006. Epub 2009 Aug 8.

DOI:10.1016/j.jaut.2009.07.006
PMID:19665867
Abstract

Cytotoxic T lymphocyte antigen-4 (CTLA4) and IgG fusion protein, CTLA4-Ig, is a therapeutic agent used for rheumatoid arthritis. It binds B7 molecules on dendritic cells (DCs) and thereby blocks B7/CD28 costimulatory interaction and inhibits effective T cell proliferation. However, the effect of CTLA4-Ig on the regulatory T cell (Treg) is still not known. In this study, we investigated the influence of CTLA4-Ig on the CD4+CD25+Foxp3+ Treg population in collagen-induced arthritis (CIA) mouse model. CTLA4-Ig suppressed CIA and increased the CD4+CD25+Foxp3+ Treg population in joint and spleen. When CD11c + DCs and CD4+T cells from CIA mice were cultured with anti-CD3, CTLA4-Ig increased the CD4+CD25 + Foxp3+ Treg population in a TGF-beta-dependent manner. When CD11c + DCs from CIA mice were treated with CTLA4-Ig and adoptively transferred into CIA-induced mice, arthritis did not develop in association with the increase in CD4+CD25+Foxp3+ Treg population. However, in CTLA4-Ig-untreated DC-transferred CIA mice, arthritis developed and then rapidly progressed. Our study demonstrated that CTLA4-Ig suppressed CIA by modifying DCs from CIA mice into tolerogenic DCs to increase the CD4+CD25+Foxp3+ Treg population and this seems to be the new immune regulatory mechanism of CTLA4-Ig.

摘要

细胞毒性 T 淋巴细胞相关抗原 4（CTLA4）和 IgG 融合蛋白，CTLA4-Ig，是一种用于类风湿关节炎的治疗药物。它与树突状细胞（DC）上的 B7 分子结合，从而阻断 B7/CD28 共刺激相互作用并抑制有效的 T 细胞增殖。然而，CTLA4-Ig 对调节性 T 细胞（Treg）的影响尚不清楚。在这项研究中，我们研究了 CTLA4-Ig 对胶原诱导性关节炎（CIA）小鼠模型中 CD4+CD25+Foxp3+Treg 群体的影响。CTLA4-Ig 抑制 CIA 并增加关节和脾脏中的 CD4+CD25+Foxp3+Treg 群体。当 CIA 小鼠的 CD11c+DC 和 CD4+T 细胞与抗 CD3 共培养时，CTLA4-Ig 以 TGF-β依赖性方式增加 CD4+CD25+Foxp3+Treg 群体。当 CIA 小鼠的 CD11c+DC 用 CTLA4-Ig 处理并过继转移到 CIA 诱导的小鼠中时，关节炎不会发展，同时 CD4+CD25+Foxp3+Treg 群体增加。然而，在未用 CTLA4-Ig 处理的 DC 转移 CIA 小鼠中，关节炎发展并迅速进展。我们的研究表明，CTLA4-Ig 通过将 CIA 小鼠的 DC 转化为耐受性 DC 来抑制 CIA，从而增加 CD4+CD25+Foxp3+Treg 群体，这似乎是 CTLA4-Ig 的新免疫调节机制。

相似文献

[1]
CTLA4-Ig modifies dendritic cells from mice with collagen-induced arthritis to increase the CD4+CD25+Foxp3+ regulatory T cell population.

J Autoimmun. 2009-8-8

[2]
CD8alpha+ dendritic cells enhance the antigen-specific CD4+ T-cell response and accelerate development of collagen-induced arthritis.

Immunol Lett. 2007-8-15

[3]
Bone marrow CD11b(+)F4/80(+) dendritic cells ameliorate collagen-induced arthritis through modulating the balance between Treg and Th17.

Int Immunopharmacol. 2015-3

[4]
Natural killer cells prevent CD28-mediated Foxp3 transcription in CD4+CD25- T lymphocytes.

Exp Hematol. 2007-3

[5]
Identification and characterization of Foxp3(+) gammadelta T cells in mouse and human.

Immunol Lett. 2009-8-15

[6]
CD4+Foxp3+ regulatory T cells converted by rapamycin from peripheral CD4+CD25(-) naive T cells display more potent regulatory ability in vitro.

Chin Med J (Engl). 2010-4-5

[7]
A distinct tolerogenic subset of splenic IDO(+)CD11b(+) dendritic cells from orally tolerized mice is responsible for induction of systemic immune tolerance and suppression of collagen-induced arthritis.

Cell Immunol. 2012-7-10

[8]
Antigen-induced, tolerogenic CD11c+,CD11b+ dendritic cells are abundant in Peyer's patches during the induction of oral tolerance to type II collagen and suppress experimental collagen-induced arthritis.

Arthritis Rheum. 2006-3

[9]
Influence of polysaccharide fractions isolated from Caltha palustris L. on the cellular immune response in collagen-induced arthritis (CIA) in mice. A comparison with methotrexate.

J Ethnopharmacol. 2012-11-1

[10]
Enhanced efficacy of regulatory T cell transfer against increasing resistance, by elevated Foxp3 expression induced in arthritic murine hosts.

Arthritis Rheum. 2007-9

引用本文的文献

[1]
The 'T paradox' in inflammatory arthritis.

Nat Rev Rheumatol. 2025-1

[2]
Augmenting regulatory T cells: new therapeutic strategy for rheumatoid arthritis.

Front Immunol. 2024

[3]
Cell-based therapies for the treatment of rheumatoid arthritis.

Immun Inflamm Dis. 2023-11

[4]
Immunomodulation for Tissue Repair and Regeneration.

Tissue Eng Regen Med. 2023-6

[5]
Localized cytotoxic T cell-associated antigen 4 and antioxidant islet encapsulation alters macrophage signaling and induces regulatory and anergic T cells to enhance allograft survival.

Am J Transplant. 2023-4

[6]
Regulatory T cells in rheumatoid arthritis: functions, development, regulation, and therapeutic potential.

Cell Mol Life Sci. 2022-9-29

[7]
CAR-T Regulatory (CAR-Treg) Cells: Engineering and Applications.

Biomedicines. 2022-1-26

[8]
Cytotoxic T lymphocyte antigen-4 regulates development of xenogenic graft versus host disease in mice via modulation of host immune responses induced by changes in human T cell engraftment and gene expression.

Clin Exp Immunol. 2021-12

[9]
Probiotic-Induced Tolerogenic Dendritic Cells: A Novel Therapy for Inflammatory Bowel Disease?

Int J Mol Sci. 2021-7-31

[10]
Immunomodulatory Therapies for the Treatment of Graft-versus-host Disease.

Hemasphere. 2021-6-1

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