Advertisement
Corrigendum
Open Access | 
10.1172/JCI171350
NLRP12 is an innate immune checkpoint for repressing IFN signatures and attenuating lupus nephritis progression
Yen-Po Tsao, Fang-Yu Tseng, Chih-Wei Chao, Ming-Han Chen, Yi-Chen Yeh, Babamale Olarewaju Abdulkareem, Se-Yi Chen, Wen-Ting Chuang, Pei-Ching Chang, I-Chun Chen, Pin-Hsuan Wang, Chien-Sheng Wu, Chang-Youh Tsai, and Szu-Ting Chen
Find articles by Tsao, Y. in: PubMed | Google Scholar
Find articles by Tseng, F. in: PubMed | Google Scholar
Find articles by Chao, C. in: PubMed | Google Scholar
Find articles by Chen, M. in: PubMed | Google Scholar
Find articles by Yeh, Y. in: PubMed | Google Scholar
Find articles by Abdulkareem, B. in: PubMed | Google Scholar
Find articles by Chen, S. in: PubMed | Google Scholar
Find articles by Chuang, W. in: PubMed | Google Scholar
Find articles by Chang, P. in: PubMed | Google Scholar
Find articles by Chen, I. in: PubMed | Google Scholar
Find articles by Wang, P. in: PubMed | Google Scholar
Find articles by Wu, C. in: PubMed | Google Scholar
Find articles by Tsai, C. in: PubMed | Google Scholar
Find articles by Chen, S. in: PubMed | Google Scholar
Published May 1, 2023 - More info
J Clin Invest. 2023;133(9):e171350. https://doi.org/10.1172/JCI171350.
© 2023 Tsao et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
Related article:
Abstract
Signaling driven by nucleic acid sensors participates in interferonopathy-mediated autoimmune diseases. NLRP12, a pyrin-containing NLR protein, is a negative regulator of innate immune activation and type I interferon (IFN-I) production. Peripheral blood mononuclear cells (PBMCs) derived from systemic lupus erythematosus (SLE) patients expressed lower levels of NLRP12, with an inverse correlation with IFNA expression and high disease activity. NLRP12 expression was transcriptionally suppressed by runt-related transcription factor 1–dependent (RUNX1-dependent) epigenetic regulation under IFN-I treatment, which enhanced a negative feedback loop between low NLRP12 expression and IFN-I production. Reduced NLRP12 protein levels in SLE monocytes was linked to spontaneous activation of innate immune signaling and hyperresponsiveness to nucleic acid stimulations. Pristane-treated Nlrp12–/– mice exhibited augmented inflammation and immune responses; and substantial lymphoid hypertrophy was characterized in NLRP12-deficient lupus-prone mice. NLRP12 deficiency mediated the increase of autoantibody production, intensive glomerular IgG deposition, monocyte recruitment, and the deterioration of kidney function. These were bound in an IFN-I signature–dependent manner in the mouse models. Collectively, we reveal a remarkable link between low NLRP12 expression and lupus progression, which suggests the impact of NLRP12 on homeostasis and immune resilience.
Authors
Yen-Po Tsao, Fang-Yu Tseng, Chih-Wei Chao, Ming-Han Chen, Yi-Chen Yeh, Babamale Olarewaju Abdulkareem, Se-Yi Chen, Wen-Ting Chuang, Pei-Ching Chang, I-Chun Chen, Pin-Hsuan Wang, Chien-Sheng Wu, Chang-Youh Tsai, Szu-Ting Chen
-
Original citation: J Clin Invest. 2023;133(3):1–19. https://doi.org/10.1172/JCI157272
Citation for this corrigendum: J Clin Invest. 2023;133(9):171350. https://doi.org/10.1172/JCI171350
Figures 1, F, J, and Q, reported incorrect P values. For Figure 5, C and E, the x axis labels were incorrect and h.p.s. was not defined. Figure 5F was missing P values. In addition, Dr. Szu-Ting Chen’s affiliations were incorrect. The correct figure parts, definition, and affiliations list are below.
h.p.s., hours post stimulation.
Yen-Po Tsao,1,2,3 Fang-Yu Tseng,4 Chih-Wei Chao,1,4 Ming-Han Chen,2 Yi-Chen Yeh,5 Babamale Olarewaju Abdulkareem,6 Se-Yi Chen,7,8 Wen-Ting Chuang,1 Pei-Ching Chang,9 I-Chun Chen,1 Pin-Hsuan Wang,1 Chien-Sheng Wu,10 Chang-Youh Tsai,2 and Szu-Ting Chen1,4,6,11
Copyright © 2025 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)