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Cell type specific IL-27p28 (IL-30) deletion uncovers an unexpected pro-inflammatory property of IL-30 in autoimmune inflammation

Dongkyun Kim, Sohee Kim, Zhinan Yin, View ORCID ProfileBooki Min
doi: https://doi.org/10.1101/2022.01.03.474823
Dongkyun Kim
1Department of Microbiology and Immunology, Northwestern University Feinberg School of Medicine, Chicago, IL, United States
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Sohee Kim
1Department of Microbiology and Immunology, Northwestern University Feinberg School of Medicine, Chicago, IL, United States
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Zhinan Yin
2Guangdong Provincial Key Laboratory of Tumor Interventional Diagnosis and Treatment, Zhuhai Institute of Translational Medicine, Zhuhai People’s Hospital Affiliated with Jinan University, Jinan University, Zhuhai, China
3The Biomedical Translational Research Institute, Faculty of Medical Science, Jinan University, Guangzhou, China
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Booki Min
1Department of Microbiology and Immunology, Northwestern University Feinberg School of Medicine, Chicago, IL, United States
4Robert H. Lurie Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL, United States
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  • ORCID record for Booki Min
  • For correspondence: booki.min@northwestern.edu
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Abstract

IL-27 is an IL-12 family cytokine with potent immunoregulatory properties, capable of modulating inflammatory responses, including autoimmunity. While extensive studies have been performed to investigate the major target cells of IL-27 mediating its functions, the source of IL-27 especially during tissue specific autoimmune inflammation has not formally been tested. IL-27p28 subunit, also known as IL-30, was initially discovered as an IL-27-specific subunit, and its expression has thus been used as a surrogate for IL-27. However, there is emerging evidence that IL-27p28 can be secreted without Ebi3, a subunit that forms IL-27 with IL-27p28. Furthermore, IL-27p28 was also reported to act as a negative regulator antagonizing IL-27. In this study, we utilized various cell type specific IL-27p28-deficient mouse models and examined the major source of IL-27p28 in T cell mediated autoimmune neuroinflammation. We found that dendritic cell-derived IL-27p28 is dispensable for the disease development but that IL-27p28 expressed by infiltrating and CNS resident APC subsets, namely, infiltrating monocytes, microglia, and astrocytes, play an essential role in limiting inflammation. Unexpectedly, we observed that cell type specific IL-27p28 deficiency expressing severe disease phenotype is associated with dysregulated IL-27p28 expression in otherwise unaffected APC subsets, suggesting that disproportionate IL-27p28 expressed may increase disease susceptibility. Indeed, systemic recombinant IL-30 administration also induced severe disease. Taken together, our results uncover a pro-inflammatory property of IL-30 that supports encephalitogenic immunity in vivo.

Competing Interest Statement

The authors have declared no competing interest.

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Posted January 03, 2022.
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Cell type specific IL-27p28 (IL-30) deletion uncovers an unexpected pro-inflammatory property of IL-30 in autoimmune inflammation
Dongkyun Kim, Sohee Kim, Zhinan Yin, Booki Min
bioRxiv 2022.01.03.474823; doi: https://doi.org/10.1101/2022.01.03.474823
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Cell type specific IL-27p28 (IL-30) deletion uncovers an unexpected pro-inflammatory property of IL-30 in autoimmune inflammation
Dongkyun Kim, Sohee Kim, Zhinan Yin, Booki Min
bioRxiv 2022.01.03.474823; doi: https://doi.org/10.1101/2022.01.03.474823

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