Transient Foxp3(+) regulatory T-cell depletion enhances protective Th1/Th17 immune response in murine sporotrichosis caused by Sporothrix schenckii

Batista-Duharte, Alexander; Téllez-Martínez, Damiana; Andrade, Cléverton Roberto de; Polesi, Marisa Campos; Portuondo, Deivys Leandro; Carlos, Iracilda Zeppone

doi:10.1016/j.imbio.2020.151993

Cited by 7 publications

(13 citation statements)

References 56 publications

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“…In S. schenckii-infected mice, an increased Tregs response was present at early period, but declined after 21 days post infection, while S. brasiiensis-infected mice showed a long lasting elevated Tregs response (35). Tregs depletion in mice was accompanied with enhanced Th1/Th17 response in schenckii-infection (36). However, Tregs profile in human sporotrichosis is still unclear.…”

Section: Discussionmentioning

confidence: 99%

Th2 Biased Immunity With Altered B Cell Profiles in Circulation of Patients With Sporotrichosis Caused by Sporothrix globosa

Yao

Song

et al. 2020

Front. Immunol.

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Section: Discussionmentioning

confidence: 99%

Th2 Biased Immunity With Altered B Cell Profiles in Circulation of Patients With Sporotrichosis Caused by Sporothrix globosa

Yao

Song

et al. 2020

Front. Immunol.

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“…The authors discuss that their results are similar to those obtained by Bozzi et al 2006, [75] who, analyzing IL-10 and TNF-α gene polymorphisms in paracoccidioidomycosis, demonstrated an association between the IL-10 polymorphism and disease. The role of regulatory T cells (Tregs) on protective immunity in fungal infections is controversial, but in some cases (such as sporotrichosis) it was recently shown that Tregs have a deleterious role, as depletion of this cell population improves the protective antifungal immunity [76]. In paracoccidioidomycosis, the role of Tregs seems to be negative, since adverse effects of this cell subpopulation were reported by various authors reporting data from experimental models and from patients.…”

Section: Cells Of the Acquired Immunitymentioning

confidence: 99%

Paracoccidioidomycosis Protective Immunity

Burger

2021

JoF

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Protective immunity against Paracoccidioides consists of a stepwise activation of numerous effector mechanisms that comprise many cellular and soluble components. At the initial phase of non-specific innate immunity, resistance against Paracoccidioides comes from phagocytic polymorphonuclear neutrophils, natural killer (NK) cells and monocytes, supplemented by soluble factors such as cytokines and complement system components. Invariant receptors (Toll-like receptors (TLRs), Dectins) which are present in cells of the immune system, detect patterns present in Paracoccidioides (but not in the host) informing the hosts cells that there is an infection in progress, and that the acquired immunity must be activated. The role of components involved in the innate immunity of paracoccidioidomycosis is herein presented. Humoral immunity, represented by specific antibodies which control the fungi in the blood and body fluids, and its role in paracoccidioidomycosis (which was previously considered controversial) is also discussed. The protective mechanisms (involving various components) of cellular immunity are also discussed, covering topics such as: lysis by activated macrophages and cytotoxic T lymphocytes, the participation of lytic products, and the role of cytokines secreted by T helper lymphocytes in increasing the efficiency of Paracoccidioides, lysis.

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“…DAB2, as a target gene for Foxp3, is required for regulating T (Treg) cell function, 11 and there is evidence that S . schenckii infection elicits an expansion of the splenic CD4 + Foxp3 + populations, 29 but the role of Tregs in fungal infection is controversial. It has been suggested by some that the immunosuppressive role of Tregs serves to avoid excessive inflammation and promotes the elimination of pathogens in advanced stages of infection, 30 while others believe Tregs exacerbate the fungal burden and inflammation in renal disease 31 …”

Section: Discussionmentioning

confidence: 99%

Sporothrix schenckii regulates macrophage inflammatory responses via the c‐JUN‐induced Dab2 transcription

Zhao

Gao

et al. 2022

Experimental Dermatology

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Macrophages, which serve as a bridge between innate and adaptive immunity, play an important role in sporotrichosis. Sporothrix schenckii infections can produce immune responses such as macrophage polarization and inflammatory factor secretion. In the early stages of inflammation, the expression of DAB2 in macrophages is increased, which controls the secretion of inflammatory factors and affects the polarization of macrophages. However, the expressions and mechanisms of DAB2 in sporotrichosis are not clear. In this study, we examined the expression of DAB2 and its regulation of inflammatory factors under conditions of Sporothrix schenckii infection. Our results indicated that the Sporothrix schenckii infection increased the expression of DAB2 and revealed a mixed M1/M2‐like type of gene expression in BMDMs with the inhibited Il‐6, Il1‐β and Arg‐1 and induced Tnf‐α, Il‐10 and Mgl‐1. The deficiency of Dab2 gene suspended the changes of cytokines. In addition, JNK activity in BMDMs was inhibited by Sporothrix schenckii infection, leading to an increase in c‐JUN. We also identified c‐JUN as a transcription factor for Dab2 through chromatin immunoprecipitation and luciferase reporter assays. In an in vivo mouse model, sporotrichosis‐induced skin lesions were accompanied with an upregulation of c‐JUN and inhibition of JNK activity, which were in accord with findings from in vitro experiments. Taken together, these findings indicate that in the early stages of Sporothrix schenckii infection there is a promotion of DAB2 expression through the JNK/c‐JUN pathway, effects that can then control the expression of inflammatory factors.

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Transient Foxp3(+) regulatory T-cell depletion enhances protective Th1/Th17 immune response in murine sporotrichosis caused by Sporothrix schenckii

Cited by 7 publications

References 56 publications

Th2 Biased Immunity With Altered B Cell Profiles in Circulation of Patients With Sporotrichosis Caused by Sporothrix globosa

Th2 Biased Immunity With Altered B Cell Profiles in Circulation of Patients With Sporotrichosis Caused by Sporothrix globosa

Paracoccidioidomycosis Protective Immunity

Sporothrix schenckii regulates macrophage inflammatory responses via the c‐JUN‐induced Dab2 transcription

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