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Mgl2 cDC2s coordinate fungal allergic airway type 2, but not type 17, inflammation in mice.
Nat Commun
January 2025
Lydia Becker Institute of Immunology and Inflammation, University of Manchester, Manchester, United Kingdom.
Fungal spores are abundant in the environment and a major cause of asthma. Originally characterised as a type 2 inflammatory disease, allergic airway inflammation that underpins asthma can also involve type 17 inflammation, which can exacerbate disease causing failure of treatments tailored to inhibit type 2 factors. However, the mechanisms that determine the host response to fungi, which can trigger both type 2 and type 17 inflammation in allergic airway disease, remain unclear.
View Article and Find Full Text PDFAnti-correlation of KLRG1 and PD-1 expression in human tumor CD8 T cells.
Oncotarget
January 2025
Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Recently, combination checkpoint therapy of cancer has been recognized as producing additive as opposed to synergistic benefit due in part to positively correlated effects. The potential for uncorrelated or negatively correlated therapies to produce true synergistic benefits has been noted. Whereas the inhibitory receptors PD-1, CTLA-4, TIM-3, LAG-3, and TIGIT have been collectively characterized as exhaustion receptors, another inhibitory receptor KLRG1 was historically characterized as a senescent receptor and received relatively little attention as a potential checkpoint inhibitor target.
View Article and Find Full Text PDFLactococcus lactis subsp. Lactis boosts stress resistance and host defense mechanisms in Caenorhabditis elegans.
J Appl Microbiol
January 2025
Graduate School of Human Life and Ecology, Osaka Metropolitan University, 3-3-138, Sugimoto, Sumiyoshi-Ku, Osaka 558-8585, Japan.
Aims: To investigate the effects of Lactococcus lactis subsp. lactis strains LL100933 and LL12007 on the host defense mechanisms of Caenorhabditis elegans against pathogenic infections and stressors.
Methods And Results: C.
The C3/C3aR pathway exacerbates acetaminophen-induced mouse liver injury via upregulating podoplanin on the macrophage.
FASEB J
January 2025
Jiangsu Institute of Hematology, National Clinical Research Center for Hematologic Diseases, NHC Key Laboratory of Thrombosis and Hemostasis, The First Affiliated Hospital of Soochow University, Suzhou, China.
Acute liver failure (ALF) is a life-threatening condition that occurs when the liver sustains severe damage and rapidly loses its function. The primary cause of ALF is the overdose of acetaminophen (APAP), and its treatment is relatively limited. The involvement of the complement system in the development of ALF has been implicated.
View Article and Find Full Text PDFRevealing the Immune Response of Gyllenhal to Entomopathogenic Fungi Infection Through Integrative Analyses of Transcriptomics and Metabolomics.
Insects
November 2024
School of Agriculture, Ningxia University, Yinchuan 750021, China.
In this study, we selected , one of the primary insect pests of alfalfa, as the experimental insect and infected it with . Transcriptomic and metabolomic analyses were conducted to explore alterations in gene expression and metabolic processes in at 48, 96, and 144 h post infection with . The transcriptomic analysis unveiled that infection boosted immune responses in tubercula, affecting carbohydrate metabolism, cytochrome P450 activity, lysosome function, apoptosis regulation, phagosome formation, glutathione metabolism, amino acid metabolism, and pathogen response pathways.
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