Dendritic cell line AP284 supports Th17 amplification

Oliveira, Paulo B.; Gomes, Clayson Moura; Ávila, Lucilla Ribeiro; Ribeiro‐Dias, Fátima; Leenen, Pieter J.M.; Oliveira, Milton Adriano Pelli de

doi:10.1016/j.cellimm.2019.02.003

Cited by 3 publications

(3 citation statements)

References 47 publications

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“…DCs, as a professional APC, are highly specialized in presenting antigens to T cells [28], followed activating CD4 + T cells can fight against the parasites by producing inflammatory cytokines, leading to activation of other immune cells and Abs production of B cell [29]. In turn, cytokines from activated DCs stimulated differentiation of distinct CD4 + T lymphocyte profiles [30,31]. IL-12 can induce generation of Th1 lymphocytes, which can control intracellular microorganisms [32][33][34].…”

Section: Discussionmentioning

confidence: 99%

Plasmodium yoelii 17XL infection modified maturation and function of dendritic cells by skewing Tregs and amplificating Th17

Chen

Nie³

et al. 2020

BMC Infect Dis

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Background: Emerging data has suggested that Tregs, Th17, Th1 and Th2 are correlated with early immune mechanisms by controlling Plasmodium infection. Plasmodium infection appeared to impair the antigen presentation and maturation of DCs, leading to attenuation of specific cellular immune response ultimately. Hence, in this study, we aim to evaluate the relevance between DCs and Tregs/Th17 populations in the process and outcomes of infection with Plasmodium yoelii 17XL (P.y17XL). Methods: DCs detection/analysis dynamically was performed by Tregs depletion or Th17 neutralization in P.y17XL infected BALB/c mice via flow cytometry. Then the levels of cytokines production were detected using enzymelinked mmunosorbent assay (ELISA). Results: Our results indicated that Tregs depletion or Th17 neutralization in BALB/c mice infected with P.y17XL significantly up-regulated the percentages of mDC and pDC, increased the expressions of major histocompatibility complex (MHC) class II, CD80, CD86 on DCs and the levels of IL-10/IL-12 secreted by DCs, indicating that abnormal amplification of Tregs or Th17 may damage the maturation and function of DCs during the early stage of malaria infection. Interestingly, we also found that the abnormal amplification of Th17, as well as Tregs, could inhibit the maturation of DCs. Conclusions: Tregs skewing or Th17 amplification during the early stage of malaria infection may inhibit the maturation and function of DCs by modifying the subsets of DCs, expressions of surface molecules on DCs and secretion mode of cytokines.

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Section: Discussionmentioning

confidence: 99%

Plasmodium yoelii 17XL infection modified maturation and function of dendritic cells by skewing Tregs and amplificating Th17

Chen

Nie³

et al. 2020

BMC Infect Dis

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“…They hold a central role in initiating, modulating, and sustaining specific immune responses. Toll-like receptors (TLRs) are a class of transmembrane proteins mainly expressed in antigen-presenting cells like DCs and macrophages ( 9 ). TLRs expressed on DC can bind to their corresponding ligands and cause DC activation ( 10 , 11 ), which are vital in the host immune system’s defense against pathogens.…”

Section: Introductionmentioning

confidence: 99%

NECA alleviates inflammatory responses in diabetic retinopathy through dendritic cell toll-like receptor signaling pathway

Li,

Chen,

Wang

et al. 2024

Front. Immunol.

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IntroductionThis study examined the impact of 5’-(N- ethylcarboxamido)adenosine (NECA) in the peripheral blood of healthy individuals, those with diabetes mellitus, diabetic retinopathy (DR), and C57BL/6 mice, both in vivo and in vitro.MethodsEnzyme-linked immunosorbent assay (ELISA) and flow cytometry (FCM) were used to evaluate the effects of NECA on dendritic cells (DCs) and mouse bone marrow-derived dendritic cells (BMDCs) and the effects of NECA-treated DCs on Treg and Th17 cells. The effect of NECA on the Toll-like receptor (TLR) pathway in DCs was evaluated using polymerase chain reaction (PCR) and western blotting (WB).ResultsFCM and ELISA showed that NECA inhibited the expression of surface markers of DCs and BMDCs, increased anti-inflammatory cytokines and decreased proinflammatory cytokines. PCR and WB showed that NCEA decreased mRNA transcription and protein expression in the TLR-4-MyD88-NF-kβ pathway in DCs and BMDCs. The DR severity in streptozocin (STZ) induced diabetic mice was alleviated. NECA-treated DCs and BMDCs were co-cultivated with CD4+T cells, resulting in modulation of Treg and Th17 differentiation, along with cytokine secretion alterations.ConclusionNECA could impair DCs’ ability to present antigens and mitigate the inflammatory response, thereby alleviating the severity of DR.

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“…18 After antigenic stimulation, naïve CD4 + T cells get activated, proliferate, and differentiate into cells with different effector phenotypes, including Th1, Th2, Th17, and regulatory T-cell lineages. 19 Several reports have implicated DC-derived Th17-promoting cytokines, such as IL-1β, IL-6, and IL-23, that are thought to promote Th17 responses that develop during bacterial and fungal infections. 20 However, whether an A. fumigatus-induced Th17 inflammatory response takes place during FK remains unknown.…”

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confidence: 99%

TSLP Produced by Aspergillus fumigatus-Stimulated DCs Promotes a Th17 Response Through the JAK/STAT Signaling Pathway in Fungal Keratitis

Han

Guo

Wang

et al. 2020

Invest. Ophthalmol. Vis. Sci.

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Purpose The purpose of this study was to explore the role of thymic stromal lymphopoietin (TSLP) secreted by Aspergillus fumigatus –stimulated dendritic cells (DCs) during the T helper 17 (Th17) immune response, and further clarify the mechanisms contributing to the Th17 immune response of fungal keratitis (FK). Methods A carboxyfluorescein diacetate succinimidyl ester assay, PCR, and flow cytometry were performed to detect Th17 differentiation of CD4 + T cells; PCR, ELISA, and Western blot were used to detect the expression of TSLP and JAK/STAT–related proteins; Signaling pathways involved in Th17 response was evaluated using RNA sequence; C57BL/6 mice were infected with A. fumigatus and treated with ruxolitinib or BBI608. Slit-lamp examination, fluorescein staining, and clinical scores were used to assess the clinical manifestation. Results A. fumigatus –infected DCs could drive naïve CD4 + T-cell proliferation and promote the production of Th17 cytokines IL-17A, IL-17F, and IL-22. A. fumigatus stimulation increased the expression of TSLP in DCs. DC-derived TSLP contributed to a Th17-type inflammatory response via the JAK/STAT signaling pathway. TSLP small interfering RNA, TSLPR small interfering RNA, or JAK/STAT inhibitors inhibited the Th17 immune response induced by A. fumigatus –infected DCs. Moreover, TSLP promoted A. fumigatus keratitis disease progression in a mouse model. However, inhibition of the JAK/STAT signaling pathway using a specific inhibitor reversed the development of FK by A. fumigatus infection. Conclusions TSLP secreted by A. fumigatus –stimulated DCs played a significant role in the Th17-dominant immune response of FK through its JAK/STAT activation. Our findings may contribute to the elucidation of the molecular mechanisms of FK and to the development of novel therapeutic approaches.

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Dendritic cell line AP284 supports Th17 amplification

Cited by 3 publications

References 47 publications

Plasmodium yoelii 17XL infection modified maturation and function of dendritic cells by skewing Tregs and amplificating Th17

Plasmodium yoelii 17XL infection modified maturation and function of dendritic cells by skewing Tregs and amplificating Th17

NECA alleviates inflammatory responses in diabetic retinopathy through dendritic cell toll-like receptor signaling pathway

TSLP Produced by Aspergillus fumigatus-Stimulated DCs Promotes a Th17 Response Through the JAK/STAT Signaling Pathway in Fungal Keratitis

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