A model of dysregulated crosstalk between dendritic, natural killer, and regulatory T cells in chronic obstructive pulmonary disease

被引:1
|
作者
Mengistu, Dawit T. [1 ]
Curtis, Jeffrey L. [1 ,2 ,3 ]
Freeman, Christine M. [1 ,2 ,4 ]
机构
[1] Univ Michigan, Grad Program Immunol, Ann Arbor, MI 48109 USA
[2] Univ Michigan Hlth Syst, Dept Internal Med, Pulm & Crit Care Med Div, Ann Arbor, MI 48109 USA
[3] VA Ann Arbor Healthcare Syst, Pulm & Crit Care Med Sect, Ann Arbor, MI USA
[4] VA Ann Arbor Healthcare Syst, Res Serv, Ann Arbor, MI 48109 USA
关键词
NK CELLS; LYMPHOID FOLLICLES; SMALL AIRWAYS; CUTTING EDGE; INFLAMMATION; ACTIVATION; EXPRESSION; SUPPRESS; DIFFERENTIATION; TRANSCRIPTION;
D O I
10.1016/j.it.2024.04.010
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Chronic obstructive pulmonary disease (COPD) is characterized by infiltration of the airways and lung parenchyma by inflammatory cells. Lung pathology results from the cumulative effect of complex and aberrant interactions between multiple cell types. However, three cell types, natural killer cells (NK), dendritic cells (DCs), and regulatory T cells (Tregs), are understudied and underappreciated. We propose that their mutual interactions significantly contribute to the development of COPD. Here, we highlight recent advances in NK, DC, and Treg biology with relevance to COPD, discuss their pairwise bidirectional interactions, and identify knowledge gaps that must be bridged to develop novel therapies. Understanding their interactions will be crucial for therapeutic use of autologous Treg, an approach proving effective in other diseases with immune components.
引用
收藏
页码:428 / 441
页数:14
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