IL-33-ST2 Axis Regulates Myeloid Cell Differentiation and Activation Enabling Effective Club Cell Regeneration

Researchers demonstrated a protective function for the IL-33-ST2 axis in bronchial epithelial repair, and implicated ST2 in myeloid cell differentiation.
[Nature Communications]
Dagher, R., Copenhaver, A. M., Besnard, V., Berlin, A., Hamidi, F., Maret, M., Wang, J., Qu, X., Shrestha, Y., Wu, J., Gautier, G., Raja, R., Aubier, M., Kolbeck, R., Humbles, A. A., & Pretolani, M. (2020). IL-33-ST2 axis regulates myeloid cell differentiation and activation enabling effective club cell regeneration. Nature Communications, 11(1), 4786. https://doi.org/10.1038/s41467-020-18466-w Cite
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DR3 Stimulation of Adipose Resident ILC2s Ameliorates Type 2 Diabetes Mellitus

Investigators established that expression of Death Receptor 3 (DR3), a member of the TNF superfamily, on visceral adipose tissue-derived murine and peripheral blood human group 2 innate lymphoid cells was inducible by IL-33.
[Nature Communications]
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A Regulatory T Cell Notch4–GDF15 Axis Licenses Tissue Inflammation in Asthma

Researchers found that interleukin-6- and STAT3 transcription factor-dependent upregulation of Notch4 receptor on lung tissue regulatory T cells was necessary for allergens and particulate matter pollutants to promote airway inflammation.
[Nature Immunology]
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Group 2 Innate Lymphoid Cells Exacerbate Amebic Liver Abscess in Mice

Researchers examined the roles of group 2 innate lymphoid cells (ILC2s) in amebic liver abscesses formation. Hepatic ILC2 numbers were significantly increased and they produced robust levels of IL-5.
[iScience]
Nakamura, R., Yoshizawa, A., Moriyasu, T., Deloer, S., Senba, M., Kikuchi, M., Koyasu, S., Moro, K., & Hamano, S. (2020). Group 2 innate lymphoid cells exacerbate amebic liver abscess in mice. IScience, 0(0). https://doi.org/10.1016/j.isci.2020.101544 Cite
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Type 2 Innate Lymphoid Cells (ILCs2) Induce CNS Demyelination in an HSV-IL-2 Mouse Model of Multiple Sclerosis

Histologic examination of infected IL-2rα-/-, IL-2rβ-/-, and IL-2rγ-/- mice showed demyelination in the CNS of IL-2rα-/- and IL-2rβ-/- mice but not in the CNS of IL-2rγ-/- infected mice.
[iScience]
Hirose, S., Jahani, P. S., Wang, S., Jaggi, U., Tormanen, K., Yu, J., Kato, M., Akbari, O., & Ghiasi, H. (2020). Type 2 innate lymphoid cells (ILCs2) induce CNS demyelination in an HSV-IL-2 mouse model of multiple sclerosis. IScience, 0(0). https://doi.org/10.1016/j.isci.2020.101549 Cite
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Tissue-Specific Features of Innate Lymphoid Cells

The authors summarize current knowledge of innate lymphoid cell (ILC) phenotypes in various tissues in mice and humans, aiming to clarify ILC immunity in distinct anatomical locations.
[Trends in Immunology]
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ILC1 Drives Intestinal Epithelial and Matrix Remodelling

Investigators developed gut organoid cocultures with type-1 innate lymphoid cells (ILC1) to dissect the impact of their accumulation in inflamed intestines. They demonstrated that murine and human ILC1 secrete transforming growth factor β1, driving expansion of CD44v6+ epithelial crypts.
[Nature Materials]
Jowett, G. M., Norman, M. D. A., Yu, T. T. L., Rosell Arévalo, P., Hoogland, D., Lust, S. T., Read, E., Hamrud, E., Walters, N. J., Niazi, U., Chung, M. W. H., Marciano, D., Omer, O. S., Zabinski, T., Danovi, D., Lord, G. M., Hilborn, J., Evans, N. D., Dreiss, C. A., … Gentleman, E. (2020). ILC1 drive intestinal epithelial and matrix remodelling. Nature Materials, 1–10. https://doi.org/10.1038/s41563-020-0783-8 Cite
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ILC1 Drive Intestinal Epithelial and Matrix Remodelling

Investigators developed gut organoid cocultures with type-1 innate lymphoid cells (ILC1) to dissect the impact of their accumulation in inflamed intestines.
[nature materials]
Jowett, G. M., Norman, M. D. A., Yu, T. T. L., Rosell Arévalo, P., Hoogland, D., Lust, S. T., Read, E., Hamrud, E., Walters, N. J., Niazi, U., Chung, M. W. H., Marciano, D., Omer, O. S., Zabinski, T., Danovi, D., Lord, G. M., Hilborn, J., Evans, N. D., Dreiss, C. A., … Gentleman, E. (2020). ILC1 drive intestinal epithelial and matrix remodelling. Nature Materials, 1–10. https://doi.org/10.1038/s41563-020-0783-8 Cite
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PPARγ Enhances ILC2 Function during Allergic Airway Inflammation via Transcription Regulation of ST2

The authors identified PPARγ as a positive regulator of lung Group 2 innate lymphoid cells (ILC2). Expression of PPARγ on ILC2 was dramatically induced upon interleukin-33 challenge.
[Mucosal Immunology]
Xiao, Q., He, J., Lei, A., Xu, H., Zhang, L., Zhou, P., Jiang, G., & Zhou, J. (2020). PPARγ enhances ILC2 function during allergic airway inflammation via transcription regulation of ST2. Mucosal Immunology, 1–11. https://doi.org/10.1038/s41385-020-00339-6 Cite
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Costello Syndrome Model Mice with a Hras G12S Mutation Are Susceptible to Develop House Dust Mite-Induced Atopic Dermatitis

Cultured HrasG12S/+ keratinocytes exhibited increased IL-33 expression after Dermatophagoides farinae stimulation.
[Cell Death & Disease]
Katata, Y., Inoue, S., Asao, A., Kobayashi, S., Terui, H., Inoue-Shibui, A., Abe, T., Niihori, T., Aiba, S., Ishii, N., Kure, S., & Aoki, Y. (2020). Costello syndrome model mice with a Hras G12S mutation are susceptible to develop house dust mite-induced atopic dermatitis. Cell Death & Disease, 11(8), 1–15. https://doi.org/10.1038/s41419-020-02845-8 Cite
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Group 2 Innate Lymphoid Cells Must Partner with the Myeloid–Macrophage Lineage for Long-Term Postviral Lung Disease

Scientists used a mouse model that applied an improved genetic definition of ILC2s via IL-7r–conditional Rora gene targeting and took advantage of a distinct progression from acute illness to chronic disease, based on a persistent type 2 immune response to respiratory infection with a natural pathogen.
[Journal of Immunology]
Wu, K., Wang, X., Keeler, S. P., Gerovac, B. J., Agapov, E. V., Byers, D. E., Gilfillan, S., Colonna, M., Zhang, Y., & Holtzman, M. J. (2020). Group 2 Innate Lymphoid Cells Must Partner with the Myeloid–Macrophage Lineage for Long-Term Postviral Lung Disease. The Journal of Immunology, 205(4), 1084–1101. https://doi.org/10.4049/jimmunol.2000181 Cite
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