CXCL13型
淋巴毒素
生物
淋巴系统
先天性淋巴细胞
免疫学
趋化因子
CD3型
病理
细胞生物学
免疫系统
医学
炎症
免疫
趋化因子受体
CD8型
作者
Javier Rangel‐Moreno,Damian M. Carragher,María de la Luz García-Hernández,Ji Young Hwang,Kim Kusser,Louise Hartson,Jay K. Kolls,Shabaana A. Khader,Troy D. Randall
摘要
Ectopic or tertiary lymphoid tissues, such as inducible bronchus-associated lymphoid tissue (iBALT), form in nonlymphoid organs after local infection or inflammation. However, the initial events that promote this process remain unknown. Here we show that iBALT formed in mouse lungs as a consequence of pulmonary inflammation during the neonatal period. Although we found CD4(+)CD3(-) lymphoid tissue-inducer cells (LTi cells) in neonatal lungs, particularly after inflammation, iBALT was formed in mice that lacked LTi cells. Instead, we found that interleukin 17 (IL-17) produced by CD4(+) T cells was essential for the formation of iBALT. IL-17 acted by promoting lymphotoxin-α-independent expression of the chemokine CXCL13, which was important for follicle formation. Our results suggest that IL-17-producing T cells are critical for the development of ectopic lymphoid tissues.
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