Single‐cell analysis reveals innate immunity dynamics in ankylosing spondylitis

• Published in: Clinical and translational medicine Vol. 11; no. 3; pp. e369 - n/a
• Main Authors: Liu, Jing, Tang, Yulong, Huang, Yan, Gao, Jian, Jiang, Shuai, Liu, Qingmei, Ma, Yanyun, Qian, Xiaolin, Qian, Feng, Reveille, John D., He, Dongyi, Zou, Hejian, Jin, Li, Zhu, Qi, Pu, Weilin, Wang, Jiucun
• Format: Journal Article
• Language: English
• Published: United States John Wiley & Sons, Inc 01.03.2021; John Wiley and Sons Inc; Wiley
• Subjects: Arthritis; Chemokines; Chinese medicine; Cytokines; Disease; Flow cytometry; Humans; Immunity, Innate - immunology; Letter to Editor; Medical research; Pathogenesis; Single-Cell Analysis - methods; Spondylitis, Ankylosing - immunology; Tumor necrosis factor-TNF
• ISSN: 2001-1326; 2001-1326
• DOI: 10.1002/ctm2.369

Many studies considered AS to be an autoimmune disease and focused on the adaptive immune responses in AS.4 Nevertheless, recent studies have classified AS as an auto-inflammatory disease, suggesting that innate immune abnormalities may play a crucial role in AS pathogenesis.5 However, the characterizations of innate immune cells, especially the myeloid cells and natural killer (NK) cells, are significantly underexplored in AS.6,7 Therefore, we performed the first single-cell sequencing study of AS focusing on monocytes and NK cells. [...]inflammatory scores composed by multiple key chemokines (Supporting Information and Figure 2B), as well as several crucial inflammatory pathways, including nuclear factor-kappa B, interleukin-17 (IL-17), TNF, and Toll-like receptor (TLR) pathways, were significantly downregulated after etanercept treatment (Figures S2B and S2C). [...]expression of those chemokines also decreased in plasma after etanercept treatment (Figure 2C). [...]we discovered that the memory-like and CD16medium/low NK cells might be involved in the pathogenesis of AS regardless of TNF-α blocker treatment, and further functional experiments are required to reveal their roles in AS pathogenesis Figure 4.