&lt;p&gt;Dendritic Cells Promote Treg Expansion but Not Th17 Generation in Response to &lt;em&gt;Talaromyces marneffei&lt;/em&gt; Yeast Cells&lt;/p&gt;

Tang, Yanping; Zhang, Hui; Xu, Hanzi; Zeng, Wen; Qiu, Ye; Tan, Chang; Tang, Shudan; Zhang, Jianquan

doi:10.2147/idr.s239906

Cited by 13 publications

(14 citation statements)

References 44 publications

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“…This confirms the previous published finding that T. marneffei yeasts do not upregulate IL-12 expression in human monocyte-derived DCs and monocyte-derived macrophages (Ngaosuwankul et al, 2008). Furthermore, our findings provide strong evidence that human Th17 cells are expanded when co-cultured with T. marneffei-stimulated monocytes or monocyte-derived DCs, in contrast to the findings from a recent study showing that murine BMDCs are unable to induce, or actually lower, the percentage of Th17 cells upon co-culture with T. marneffei (Tang et al, 2020). These observations point to the possible difference in Th1 and Th17 immune response towards T. marneffei in human vs murine hosts.…”

Section: Discussioncontrasting

confidence: 55%

NLRP3 inflammasome contributes to host defense againstTalaromyces marneffeiinfection

Chan

Tan

et al. 2020

Preprint

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Talaromyces marneffei is an important thermally dimorphic pathogen causing disseminated mycoses in immunocompromised individuals in southeast Asia. Previous study has suggested that NLRP3 inflammasome plays a critical role in antifungal immunity. However, the mechanism underlying the role of NLRP3 inflammasome activation in host defense against T. marneffei remains unclear. We show that T. marneffei yeasts but not conidia induce potent IL-1beta response, which is differentially regulated in discrete immune cell types. Dectin-1/Syk signaling pathway mediates pro-IL-1beta production, and NLRP3 inflammasome is activated to trigger the processing of pro-IL-1beta into IL-1beta. The activated NLRP3 inflammasome partially promotes Th1 and Th17 immune responses against T. marneffei yeasts. In vivo, mice with NLRP3 or caspase-1 deficiency exhibit higher mortality rate and fungal load compared to wild-type mice. Herein, our study provides the first evidence that NLRP3 inflammasome contributes to host defense against T. marneffei infection, which may have implications for future antifungal therapeutic designs.

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Section: Discussioncontrasting

confidence: 55%

NLRP3 inflammasome contributes to host defense againstTalaromyces marneffeiinfection

Chan

Tan

et al. 2020

Preprint

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“…At the same time macrophages can also secrete high level co-stimulating molecule CD80/CD86 as antigen-presenting cells (APCs), binding with corresponding ligands on the surface of Th cells, promoting cytotoxic T cell activation and thus eliminate T. marneffei . 5 …”

Section: Introductionmentioning

confidence: 99%

The Effect of Talaromyces marneffei Infection on CD86 Expression in THP-1 Cells

Yang¹,

Shen²,

Chen³

et al. 2021

IDR

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Background Talaromyces marneffei ( T. marneffei ) is a destructive opportunistic dimorphic fungal which can cause lethiferous Talaromycosis, but the clearance of T. marneffei mainly depends on the innate immune response. Objective To investigate whether T. marneffei can inhibit the expression of CD86 in THP-1 cells after infection and discuss the potential mechanisms. Methods Western blot and immunoelectron microscopy were used to detect the CD86 expression on T. marneffei cultured on BHI medium at 37°C. Western blot, enzyme-linked immunoassay and immunofluorescence were used to detect the change of CD86 expression on macrophages incubating with T. marneffei . Enzyme-linked immunoassay was used to detect the content of CD86 in supernatant in the co-culture system. Immunohistochemistry and immunoelectron microscopy were used to detect the expression of CD86 on T. marneffei incubating with macrophages. Results T. marneffei did not express CD86 when cultured separately at 37°C detected by Western blot and immunoelectron microscopy, but it did express CD86 when incubated with macrophages detected by immunohistochemistry and immunoelectron microscopy. The CD86 expression of macrophages significantly decreased at 72 hours when infected with T. marneffei while the content of CD86 in supernatant significantly increased at 72 hours compared with the control group which were detected by Western blot, enzyme-linked immunoassay and immunofluorescence. Conclusion 1) After T. marneffei infection, CD86 expression on THP-1 decreased, and with the progression of infection, insufficient polarization of M1 macrophages gradually appeared; 2) T. marneffei may adsorb or uptake CD86 in supernatant produced by macrophages during the contact with THP-1 cells, thus leading to the consumption of CD86 in macrophages.

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“…With T.marneffei infection macrophage pattern recognition receptors and risk-related molecular pattern receptors are activated, secreting a variety of anti-in ammatory factors, and up-regulating CD86 on macrophages which is bene cial for host elimination of T.marneffei. At the same time macrophages can also secrete high level co-stimulating molecule CD80/CD86 as antigen presenting cells (APCs), binding with corresponding ligands on the surface of Th cells, promoting cytotoxic T cell activation and thus eliminate T.marneffei [5] .…”

Section: Introductionmentioning

confidence: 99%

The Effect of Talaromyces Marneffei Infection on CD86 Expression in THP-1 Cells

Yang

Lin

Chen

et al. 2020

Preprint

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Background: Talaromyces Marneffei (T.marneffei) is an destructive opportunistic dimorphic fungal which can cause lethiferous Talaromycosis, but the clearance of T.marneffei mainly depends on the innate immune response. Objectives: To investigate the effect of T.marneffei on CD86 expression in THP-1 cells after infection and discuss the potential mechanisms. Methods: Western blot and immunoelectron microscopy were used to detect the CD86 expression on T.marneffei cultured on BHI medium at 37℃. Western blot、enzyme-linked immunoassay and immunofluorescence were used to detect the change of CD86 expression on macrophages incubating with T.marneffei. Enzyme-linked immunoassay was used to detect the content of CD86 in supernatant in the co-culture system. Immunohistochemistry and immunoelectron microscopy were used to detect the expression of CD86 on T.marneffei incubating with macrophages. Results: T.marneffei didn’t express CD86 when cultured separately at 37℃ detected by western blot and immunoelectron microscopy, but it did express CD86 when incubated with macrophages detected by immunohistochemistry and immunoelectron microscopy. The CD86 expression of macrophages significantly decreased at 72 hours when infected with T.marneffei while the content of CD86 in supernatant significantly increased at 72 hours compared with the control group which were detected by western blot, enzyme-linked immunoassay and immunofluorescence. Conclusion: 1.After T.marneffei infection，CD86 expression on THP-1 decreased，and with the progression of infection, insufficient polarization of M1 macrophages gradually appeared；2.T.marneffei may adsorb or uptake CD86 in supernatant produced by macrophages during the contact with THP-1 cells, thus leading to the consumption of CD86 in macrophages.

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<p>Dendritic Cells Promote Treg Expansion but Not Th17 Generation in Response to <em>Talaromyces marneffei</em> Yeast Cells</p>

Cited by 13 publications

References 44 publications

NLRP3 inflammasome contributes to host defense againstTalaromyces marneffeiinfection

NLRP3 inflammasome contributes to host defense againstTalaromyces marneffeiinfection

The Effect of Talaromyces marneffei Infection on CD86 Expression in THP-1 Cells

The Effect of Talaromyces Marneffei Infection on CD86 Expression in THP-1 Cells

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