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Interleukin-22 (IL-22) acts protectively and harmfully on intestinal tissue depending on the situation; therefore, IL-22 signaling needs to be tightly regulated. IL-22 binding protein (IL-22BP) binds IL-22 to inhibit IL-22 signaling. It is expressed in intestinal and lymphoid tissues, although its precise distribution and roles have remained unclear. In this study, we show that IL-22BP is highly expressed by CD11bCD8α dendritic cells in the subepithelial dome region of Peyer's patches (PPs). We found that IL-22BP blocks IL-22 signaling in the follicle-associated epithelium (FAE) covering PPs, indicating that IL-22BP plays a role in regulating the characteristics of the FAE. As expected, FAE of IL-22BP-deficient () mice exhibited altered properties such as the enhanced expression of mucus and antimicrobial proteins as well as prominent fucosylation, which are normally suppressed in FAE. Additionally, mice exhibited the decreased uptake of bacterial antigens into PPs without affecting M cell function. Our present study thus demonstrates that IL-22BP promotes bacterial uptake into PPs by influencing FAE gene expression and function.
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http://dx.doi.org/10.1084/jem.20160770 | DOI Listing |
Vulvovaginal candidiasis (VVC), caused by the commensal pathobiont affects >75% of women, marring quality of life and incurring significant health costs. Estrogen (E2) activity is tightly linked to VVC susceptibility, and preclinical models employ E2 to establish vaginal colonization. Unlike most forms of candidiasis, VVC is not considered to be a condition of immune compromise.
View Article and Find Full Text PDFViruses
August 2025
State Key Laboratory of Virology and Biosafety, Department of Infectious Diseases, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan 430071, China.
Persistent type I interferon (IFN-I) signaling compromises adaptive anti-HIV-1 T cell immunity and promotes viral reservoir persistence, yet its effects on innate lymphoid cells during chronic infection remain unclear. Through integrated single-cell RNA sequencing and functional validation in HIV-1-infected humanized mice with combination antiretroviral therapy (cART) and IFN-I signaling blockade, we reveal IFN-I-induced dysfunction of natural killer (NK) cells and group 3 innate lymphoid cells (ILC3s). Mechanistically, the IFN-I-CD9 axis drives NK cells toward a decidual NK cell-like phenotype, impairing their cytotoxic activity.
View Article and Find Full Text PDFJ Endod
August 2025
The Kishen Lab, Dental Research Institute, University of Toronto, Toronto, Canada; Faculty of Dentistry, University of Toronto, Toronto, Canada. Electronic address:
Root resorption is a pathological process characterized by the breakdown of dentin and cementum by odontoclasts, mirroring the mechanisms of osteoclast-driven bone resorption. Osteoclastogenesis is tightly regulated by the RANK/RANKL/OPG axis and other signaling pathways, including Wnt, ATP-P2RX7-IL-1, programmed cell death, and inflammasome activation. Pro-inflammatory mediators such as IL-1, IL-6, IL-8, TNF-α, IL-17, IL-22, and IL-23 drive odontoclastic differentiation, whereas anti-inflammatory cytokines, including IL-4, IL-10, and TGF-β, counteract resorptive activity.
View Article and Find Full Text PDFJ Neurotrauma
August 2025
Department of Neurosurgery, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.
Traumatic brain injury (TBI) disrupts the intestinal barrier, linking brain trauma to systemic inflammation and secondary complications. This study investigated the role of gut microbiota and its metabolites in intestinal barrier dysfunction following TBI, using a controlled cortical impact mouse model. TBI-induced gut dysbiosis was characterized by reduced microbial diversity and a loss of butyrate-producing bacteria, which led to decreased levels of short-chain fatty acids (SCFAs), particularly butyric acid.
View Article and Find Full Text PDFAllergy
August 2025
Department of Dermatology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Background: Eczematous eruption (EE) is an adverse effect observed in psoriasis patients undergoing interleukin (IL)-17A inhibitor therapy, with reported incidence rates ranging from 2.2% to 12.1%.
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