Biological function of type 1 regulatory cells and their role in type 1 diabetes

被引:0
|
作者
Qi, Lingli [1 ]
Wang, Zhichao [2 ]
Huang, Xinxing [1 ]
Gao, Xiuzhu [3 ]
机构
[1] First Hosp Jilin Univ, Childrens Med Ctr, Dept Gastroenterol, Changchun, Peoples R China
[2] First Hosp Jilin Univ, Childrens Med Ctr, Dept Surg, Changchun, Peoples R China
[3] First Hosp Jilin Univ, Dept Publ Lab Platform, Changchun, Peoples R China
关键词
Autoimmune disease; Biological function; Cell therapy; Type; 1; diabetes; Type 1 regulatory cell; CD4(+) T-CELLS; TR1; CELLS; B-CELLS; INTERLEUKIN-10; RESPONSES; FOXP3(-); IL-10; SUPPRESSION; PANCREAS; RECEPTOR;
D O I
10.1016/j.heliyon.2024.e36524
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
The collapse of immune homeostasis induces type 1 diabetes (T1D). In T1D, uncontrolled immune attacks against islet (3 cells reduce insulin secretion, resulting in hyperglycaemia and various complications. Type 1 regulatory (Tr1) cell therapy is a promising approach for the treatment of T1D. Tr1 cells are a subset of regulatory T (Treg) cells that are characterised by high interleukin10 secretion and forkhead box protein P3 non-expression. Tr1 cells are reduced and have impaired function in patients with T1D. Immunotherapy is used to treat various diseases, and Treg cells have been applied to treat T1D in animal models and clinical trials. However, the safety and efficacy of Tr1 cells in treating diabetes and other diseases remain unclear. In this review, we aim to investigate the identification and biological function of Tr1 cells and related studies on immune diseases; additionally, we discuss the feasibility, limitations, and possible solutions of Tr1 cell therapy in T1D. This review shows that T1D is caused by an immune imbalance where defective Tr1 cells fail to control effector T cells, leading to the destruction of islet (3 cells. However, Tr1 cell therapy is safe and effective for other immune diseases, suggesting its potential for treating T1D.
引用
收藏
页数:9
相关论文
共 50 条
  • [1] Regulatory B Cells: Role in Type 1 Diabetes
    Boldison, Joanne
    Wong, F. Susan
    FRONTIERS IN IMMUNOLOGY, 2021, 12
  • [2] Revisiting regulatory T cells in type 1 diabetes
    Zhang, Yuxia
    Bandala-Sanchez, Esther
    Harrison, Leonard C.
    CURRENT OPINION IN ENDOCRINOLOGY DIABETES AND OBESITY, 2012, 19 (04) : 271 - 278
  • [3] The role of B cells in the pathogenesis of type 1 diabetes
    Wang, Ya-nan
    Li, Ruihua
    Huang, Yaxuan
    Chen, Hui
    Nie, Hao
    Liu, Lian
    Zou, Xiaoting
    Zhong, Jixin
    Zheng, Bing
    Gong, Quan
    FRONTIERS IN IMMUNOLOGY, 2024, 15
  • [4] Restoring Regulatory T Cells in Type 1 Diabetes
    Spence, Allyson
    Tang, Qizhi
    CURRENT DIABETES REPORTS, 2016, 16 (11)
  • [5] The Role of Regulatory T Cells in Type 1 Diabetes
    Vieira, Margarida
    Neves, Celestino
    Neves, Joao Sergio
    Carvalho, Davide
    REVISTA PORTUGUESA DE ENDOCRINOLOGIA DIABETES E METABOLISMO, 2020, 15 (3-4) : 162 - 167
  • [6] Proinflammatory cytokines contribute to development and function of regulatory T cells in type 1 diabetes
    Thomas, Helen E.
    Graham, Kate L.
    Chee, Jonathan
    Thomas, Ranjeny
    Kay, Thomas W.
    Krishnamurthy, Balasubramanian
    TRANSLATIONAL IMMUNOLOGY IN ASIA-OCEANIA, 2013, 1283 : 81 - 86
  • [7] Type 1 diabetes and T regulatory cells
    ElEssawy, Basset
    Li, Xian C.
    PHARMACOLOGICAL RESEARCH, 2015, 98 : 22 - 30
  • [8] Autologous Regulatory T Cells for the Treatment of Type 1 Diabetes
    Thompson, James A.
    Perry, Daniel
    Brusko, Todd M.
    CURRENT DIABETES REPORTS, 2012, 12 (05) : 623 - 632
  • [9] Role of regulatory T cells in Schistosoma-mediated protection against type 1 diabetes
    Tang, Chun-lian
    Gao, Yan-ru
    Wang, Li-xia
    Zhu, Ya-wen
    Pan, Qun
    Zhang, Rong-hui
    Xiong, Ying
    MOLECULAR AND CELLULAR ENDOCRINOLOGY, 2019, 491
  • [10] Role of regulatory T cells for the treatment of type 1 diabetes Mellitus
    Jaeckel, E.
    Mpofu, N.
    Saal, N.
    Manns, M. P.
    HORMONE AND METABOLIC RESEARCH, 2008, 40 (02) : 126 - 136