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IFN-γ and IL-17 elicit synergistic anti-mycobacterial responses by inhibiting coronin-1A retention

IFN-γ and IL-17 elicit synergistic anti-mycobacterial responses by inhibiting coronin-1A retention

 Nature 2025
 Eng
Mô tả biểu ghi
ID:33954
NLM B2
Tác giả CN Phạm Thúy An
Nhan đề IFN-γ and IL-17 elicit synergistic anti-mycobacterial responses by inhibiting coronin-1A retention
Thông tin xuất bản 2025
Thông tin xuất bản Nature
Tóm tắt This study demonstrates that the downregulation of coronin-1A retention on the phagosome is a synergistic pathway for IFN-γ and IL-17 that kills Mycobacterium tuberculosis (Mtb) in macrophages. IL-17 alone does not play a role in intracellular Mtb killing but potentiates the anti-mycobactericidal pathway of IFN-γ. Co-treatment of IFN-γ/IL-17 inhibited phosphorylation of STAT3, induced LRG47 expression, and reduced retention of coronin-1A on phagosome, thereby eliciting phagolysosomal fusion and bacterial killing, which was proved through response analysis of IFN-γ/IL-17 in Mtb-infected macrophages transfected with small interfering RNA of coro1a, lrg47, or stat1. Determination of adjunctive therapeutic effect of IFN-γ, IL-17, or both with anti-mycobacterial drugs showed that the bacterial load in the tissue of mice co-treated with IFN-γ/IL-17, even at 1 ng/mL concentration each, was more rapidly reduced compared to those of IFN-γ injection or chemotherapy alone. It inhibited the re-growth after treatment termination
Thuật ngữ chủ đề Public health
Từ khóa tự do Anti-mycobacterial; Inhibiting coronin-1A retention
Địa chỉ 100Kho Bài báo quốc tế(1): BQT00041
Tệp tin điện tử https://www.nature.com/articles/s42003-025-09277-0
Tệp tin điện tử https://lib.hpmu.edu.vn/kiposdata2/tapchi2026/anhbiatc/biabbqt_thumbimage.jpg
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041[ ] |a Eng
084[ ] |a B2
100[ ] |a Phạm Thúy An
245[ ] |a IFN-γ and IL-17 elicit synergistic anti-mycobacterial responses by inhibiting coronin-1A retention
260[ ] |c 2025
260[ ] |b Nature
520[ ] |a This study demonstrates that the downregulation of coronin-1A retention on the phagosome is a synergistic pathway for IFN-γ and IL-17 that kills Mycobacterium tuberculosis (Mtb) in macrophages. IL-17 alone does not play a role in intracellular Mtb killing but potentiates the anti-mycobactericidal pathway of IFN-γ. Co-treatment of IFN-γ/IL-17 inhibited phosphorylation of STAT3, induced LRG47 expression, and reduced retention of coronin-1A on phagosome, thereby eliciting phagolysosomal fusion and bacterial killing, which was proved through response analysis of IFN-γ/IL-17 in Mtb-infected macrophages transfected with small interfering RNA of coro1a, lrg47, or stat1. Determination of adjunctive therapeutic effect of IFN-γ, IL-17, or both with anti-mycobacterial drugs showed that the bacterial load in the tissue of mice co-treated with IFN-γ/IL-17, even at 1 ng/mL concentration each, was more rapidly reduced compared to those of IFN-γ injection or chemotherapy alone. It inhibited the re-growth after treatment termination
650[ ] |a Public health
653[ ] |a Anti-mycobacterial
653[ ] |a Inhibiting coronin-1A retention
773[ ] |t Communications Biology
852[ ] |a 100 |b Kho Bài báo quốc tế |j (1): BQT00041
856[ ] |u https://www.nature.com/articles/s42003-025-09277-0
856[1 ] |u https://lib.hpmu.edu.vn/kiposdata2/tapchi2026/anhbiatc/biabbqt_thumbimage.jpg
890[ ] |a 1 |b 0 |c 0 |d 0
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