Talaromyces marneffei promotes M2-like polarization of human macrophages by downregulating SOCS3 expression and activating the TLR9 pathway
Little is known about how Talaromyces marneffei, a thermally dimorphic fungus that causes substantial morbidity and mortality in Southeast Asia, evades the human immune system. Polarization of macrophages into fungal-inhibiting M1-like and fungal-promoting M2-like types has been shown to play an imp...
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Published in | Virulence Vol. 12; no. 1; pp. 1997 - 2012 |
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Main Authors | , , , , , , , , , , , , , , , |
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01.12.2021
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Abstract | Little is known about how Talaromyces marneffei, a thermally dimorphic fungus that causes substantial morbidity and mortality in Southeast Asia, evades the human immune system. Polarization of macrophages into fungal-inhibiting M1-like and fungal-promoting M2-like types has been shown to play an important role in the innate immune response against fungal pathogens. This mechanism has not been defined for T. marneffei. Here, we demonstrated that T. marneffei promotes its survival in human macrophages by inducing them toward M2-like polarization. Our investigations of the mechanism revealed that T. marneffei infection led to SOCS3 protein degradation by inducing tyrosine phosphorylation, thereby relieving the inhibitory effect of SOCS3 on p-STAT6, a key factor for M2-like polarization. Our SOCS3-overexpression experiments showed that SOCS3 is a positive regulator of M1-like polarization and plays an important role in limiting M2-like polarization. Furthermore, we found that inhibition of the TLR9 pathway partially blocked T. marneffei-induced M2-like polarization and significantly enhanced the killing activity of macrophages against T. marneffei. Collectively, these results reveal a novel mechanism by which T. marneffei evades the immune response of human macrophages. |
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AbstractList | Little is known about how
Talaromyces marneffei
, a thermally dimorphic fungus that causes substantial morbidity and mortality in Southeast Asia, evades the human immune system. Polarization of macrophages into fungal-inhibiting M1-like and fungal-promoting M2-like types has been shown to play an important role in the innate immune response against fungal pathogens. This mechanism has not been defined for
T. marneffei
. Here, we demonstrated that
T. marneffei
promotes its survival in human macrophages by inducing them toward M2-like polarization. Our investigations of the mechanism revealed that
T. marneffei
infection led to SOCS3 protein degradation by inducing tyrosine phosphorylation, thereby relieving the inhibitory effect of SOCS3 on p-STAT6, a key factor for M2-like polarization. Our SOCS3-overexpression experiments showed that SOCS3 is a positive regulator of M1-like polarization and plays an important role in limiting M2-like polarization. Furthermore, we found that inhibition of the TLR9 pathway partially blocked
T. marneffei
-induced M2-like polarization and significantly enhanced the killing activity of macrophages against
T. marneffei
. Collectively, these results reveal a novel mechanism by which
T. marneffei
evades the immune response of human macrophages. Little is known about how Talaromyces marneffei, a thermally dimorphic fungus that causes substantial morbidity and mortality in Southeast Asia, evades the human immune system. Polarization of macrophages into fungal-inhibiting M1-like and fungal-promoting M2-like types has been shown to play an important role in the innate immune response against fungal pathogens. This mechanism has not been defined for T. marneffei. Here, we demonstrated that T. marneffei promotes its survival in human macrophages by inducing them toward M2-like polarization. Our investigations of the mechanism revealed that T. marneffei infection led to SOCS3 protein degradation by inducing tyrosine phosphorylation, thereby relieving the inhibitory effect of SOCS3 on p-STAT6, a key factor for M2-like polarization. Our SOCS3-overexpression experiments showed that SOCS3 is a positive regulator of M1-like polarization and plays an important role in limiting M2-like polarization. Furthermore, we found that inhibition of the TLR9 pathway partially blocked T. marneffei-induced M2-like polarization and significantly enhanced the killing activity of macrophages against T. marneffei. Collectively, these results reveal a novel mechanism by which T. marneffei evades the immune response of human macrophages. Little is known about how , a thermally dimorphic fungus that causes substantial morbidity and mortality in Southeast Asia, evades the human immune system. Polarization of macrophages into fungal-inhibiting M1-like and fungal-promoting M2-like types has been shown to play an important role in the innate immune response against fungal pathogens. This mechanism has not been defined for . Here, we demonstrated that promotes its survival in human macrophages by inducing them toward M2-like polarization. Our investigations of the mechanism revealed that infection led to SOCS3 protein degradation by inducing tyrosine phosphorylation, thereby relieving the inhibitory effect of SOCS3 on p-STAT6, a key factor for M2-like polarization. Our SOCS3-overexpression experiments showed that SOCS3 is a positive regulator of M1-like polarization and plays an important role in limiting M2-like polarization. Furthermore, we found that inhibition of the TLR9 pathway partially blocked -induced M2-like polarization and significantly enhanced the killing activity of macrophages against . Collectively, these results reveal a novel mechanism by which evades the immune response of human macrophages. |
Author | Luo, Qiang Li, Zhen Zhang, Hong Wang, Gang Le, Thuy Jiang, Junjun Liao, Yanyan Lai, Jingzhen Liang, Hao Wei, Wudi Liang, Bingyu Han, Jing He, Jinhao Huang, Jiegang Ye, Li Ning, Chuanyi |
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Keywords | SOCS3 TLR9 pathway macrophages Talaromyces marneffei M2 polarization |
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Snippet | Little is known about how Talaromyces marneffei, a thermally dimorphic fungus that causes substantial morbidity and mortality in Southeast Asia, evades the... Little is known about how , a thermally dimorphic fungus that causes substantial morbidity and mortality in Southeast Asia, evades the human immune system.... Little is known about how Talaromyces marneffei , a thermally dimorphic fungus that causes substantial morbidity and mortality in Southeast Asia, evades the... |
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SubjectTerms | Cell Polarity Humans Immune Evasion Immunity, Innate M2 polarization macrophages Macrophages - immunology Macrophages - microbiology Mycoses - immunology Research Paper SOCS3 Suppressor of Cytokine Signaling 3 Protein - genetics Suppressor of Cytokine Signaling 3 Protein - immunology Talaromyces - genetics Talaromyces - pathogenicity Talaromyces marneffei TLR9 pathway Toll-Like Receptor 9 - immunology |
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Title | Talaromyces marneffei promotes M2-like polarization of human macrophages by downregulating SOCS3 expression and activating the TLR9 pathway |
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