Elsevier eBooks, Год журнала: 2024, Номер unknown
Опубликована: Янв. 1, 2024
Язык: Английский
Elsevier eBooks, Год журнала: 2024, Номер unknown
Опубликована: Янв. 1, 2024
Язык: Английский
Trends in Immunology, Год журнала: 2025, Номер unknown
Опубликована: Март 1, 2025
Язык: Английский
Процитировано
0Frontiers in Immunology, Год журнала: 2024, Номер 15
Опубликована: Окт. 21, 2024
S100A9, a multifunctional protein mainly expressed by neutrophils and monocytes, poses an immunological paradox. In virus infections or sterile inflammation, it functions as alarmin attracting innate immune cells, well mediating proinflammatory effects through TLR4 signaling. However, in cancer, S100A9 levels have been shown to associate with poor prognosis lack of response immunotherapy. Its expression myeloid cells has related suppressive phenotype, the so-called derived suppressor (MDSCs). Targeting cancer therefore proposed potential way relieve myeloid-mediated suppression. Surprisingly, we found that blocking extracellular signaling from using inhibitor Paquinimod, resulted increased tumor growth detrimental effect on anti-PD-L1 efficacy CT26 model. This was caused reduction infiltration about half untreated controls, made up 5-fold decrease Ly6C high monocytic cells. The Ly6G + compartment not reduced Paquinimod treatment, suggesting alternative mechanisms which contributes Intratumoral injection recombinant early after mice inoculation had anti-tumor effect. These findings indicate important yet understudied role stimulatory signal settings, highlight exploit such signals promote beneficial responses.
Язык: Английский
Процитировано
2Biomedicines, Год журнала: 2024, Номер 12(12), С. 2889 - 2889
Опубликована: Дек. 19, 2024
Hemorrhagic shock is caused by rapid loss of a significant blood volume, which leads to insufficient flow and oxygen delivery organs tissues, resulting in severe physiological derangements, organ failure, death. Physiologic derangements after hemorrhage are due large part the body’s strong inflammatory response, immune dysfunction, secondary complications such as chronic immunosuppression, increased susceptibility infection, coagulopathy, multiple unregulated inflammation. Immediate management hemorrhagic includes timely control source bleeding, restoring intravascular preferably with whole blood, prevention ischemia failure optimizing tissue oxygenation. However, currently, there no clinically effective treatments available that can stabilize response reinstate homeostatic conditions. In this review, we will discuss what known about immunologic dysfunction following potential therapeutic strategies.
Язык: Английский
Процитировано
1bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown
Опубликована: Июнь 8, 2024
Abstract Preeclampsia (PE), a major cause of maternal and perinatal mortality with highly heterogeneous causes symptoms, is usually complicated by gestational diabetes mellitus (GDM). However, comprehensive understanding the immune microenvironment in placenta PE differences between GDM still lacking. In this study, Cytometry time flight (CyTOF) indicated that frequencies memory-like Th17 cells (CD45RA - CCR7 + IL-17A CD4 ), CD8 T (CD38 CXCR3 Helios CD127 ) pro-inflam Macs (CD206 CD163 CD38 mid CD107a low CD86 HLA-DR CD14 were increased, while anti-inflam CD33 granulocyte myeloid-derived suppressor (gMDSCs, CD11b CD15 hi decreased compared NP, but not or GDM&PE. The positively correlated negatively gMDSCs. Single-cell RNA sequencing revealed transferring F4/80 CD206 Folr2 Ccl7 Ccl8 C1qa C1qb C1qc phenotype from uterus mice to normal pregnant induced production IL-17a Rora Il1r1 TNF Cxcr6 S100a4 CD44 via IGF1-IGF1R, which contributed development recurrence PE. Pro-inflam also inhibited Ly6g S100a8 S100a9 Retnlg Wfdc21 gMDSCs at maternal-fetal interface, leading PE-like symptoms mice. conclusion, study PE-specific cell network, was regulated Macs, providing new ideas about pathogenesis
Язык: Английский
Процитировано
0eLife, Год журнала: 2024, Номер 13
Опубликована: Сен. 11, 2024
Preeclampsia (PE), a major cause of maternal and perinatal mortality with highly heterogeneous causes symptoms, is usually complicated by gestational diabetes mellitus (GDM). However, comprehensive understanding the immune microenvironment in placenta PE differences between GDM still lacking. In this study, cytometry time flight indicated that frequencies memory-like Th17 cells (CD45RA − CCR7 + IL-17A CD4 ), CD8 T (CD38 CXCR3 Helios CD127 ) pro-inflam Macs (CD206 CD163 CD38 mid CD107a low CD86 HLA-DR CD14 were increased, while anti-inflam CD33 granulocyte myeloid-derived suppressor (gMDSCs, CD11b CD15 hi decreased compared normal pregnancy (NP), but not or GDM&PE. The positively correlated negatively gMDSCs. Single-cell RNA sequencing revealed transferring F4/80 CD206 Folr2 Ccl7 Ccl8 C1qa C1qb C1qc phenotype from uterus mice to pregnant induced production IL-17a Rora Il1r1 TNF Cxcr6 S100a4 CD44 via IGF1–IGF1R, which contributed development recurrence PE. Pro-inflam also inhibited Ly6g S100a8 S100a9 Retnlg Wfdc21 gMDSCs at maternal–fetal interface, leading PE-like symptoms mice. conclusion, study PE-specific cell network, was regulated Macs, providing new ideas about pathogenesis
Язык: Английский
Процитировано
0Elsevier eBooks, Год журнала: 2024, Номер unknown
Опубликована: Янв. 1, 2024
Язык: Английский
Процитировано
0