Role of Treg, Breg and other cytokine sets in host protection and immunopathology during human leishmaniasis: Are they potential valuable markers in clinical settings and vaccine evaluation?

Divenuto, Francesca; Pavia, Grazia; Marascio, Nadia; Barreca, Giorgio Settimo; Quirino, Angela; Matera, Giovanni

doi:10.1016/j.actatropica.2023.106849

Cited by 8 publications

(14 citation statements)

References 45 publications

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“…The IL-10 produced by Tregs suppresses the proliferation of antigen-specific T-cells and decreases the production of type 1 cytokines such as IFN-γ and IL-12. This renders macrophages less responsive to IFN-γ-mediated intracellular killing [ 127 , 128 ]. M1 macrophages produce pro-inflammatory cytokines associated with the expression of inflammatory mediators such as inducible nitric oxide synthase (iNOS) and interleukin-12 (IL-12), which can trigger self-tissue damage.…”

Section: Leishmaniasis: Immune Cells Crosstalk In Macrophage Polariza...mentioning

confidence: 99%

“…During visceral leishmaniasis, IL-10 plays a crucial role in the immunosuppressive phase of the disease: high levels of this cytokine have been detected in patients with VL. It can lead to a fatal outcome in untreated cases of visceral leishmaniasis [ 127 ]. In this way, Tregs may assist in parasite persistence by suppressing macrophage activation and helping the parasite evade the host immune response through the secretion of IL-10 and TGF-β, ultimately resulting in increased host susceptibility and parasite durability [ 127 , 135 , 136 ].…”

Section: Leishmaniasis: Immune Cells Crosstalk In Macrophage Polariza...mentioning

confidence: 99%

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Leishmaniasis: Immune Cells Crosstalk in Macrophage Polarization

et al. 2023

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Leishmaniasis is a complex infectious parasitic disease caused by protozoa of the genus Leishmania, belonging to a group of neglected tropical diseases. It establishes significant global health challenges, particularly in socio-economically disadvantaged regions. Macrophages, as innate immune cells, play a crucial role in initiating the inflammatory response against the pathogens responsible for this disease. Macrophage polarization, the process of differentiating macrophages into pro-inflammatory (M1) or anti-inflammatory (M2) phenotypes, is essential for the immune response in leishmaniasis. The M1 phenotype is associated with resistance to Leishmania infection, while the M2 phenotype is predominant in susceptible environments. Notably, various immune cells, including T cells, play a significant role in modulating macrophage polarization by releasing cytokines that influence macrophage maturation and function. Furthermore, other immune cells can also impact macrophage polarization in a T-cell-independent manner. Therefore, this review comprehensively examines macrophage polarization’s role in leishmaniasis and other immune cells’ potential involvement in this intricate process.

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Section: Leishmaniasis: Immune Cells Crosstalk In Macrophage Polariza...mentioning

confidence: 99%

Section: Leishmaniasis: Immune Cells Crosstalk In Macrophage Polariza...mentioning

confidence: 99%

Leishmaniasis: Immune Cells Crosstalk in Macrophage Polarization

et al. 2023

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“…The IL-10 produced by Tregs suppresses the proliferation of antigen-specific T-cells and decreases the production of type 1 cytokines such as IFN-γ and IL-12. This renders macrophages less responsive to IFN-γ-mediated intracellular killing [118,119]. M1 macrophages produce pro-inflammatory cytokines, which are associated with the expression of inflammatory mediators such as inducible nitric oxide synthase (iNOS) and interleukin-12 (IL-12), which can trigger self-tissue damage, while Tregs limit the consequences of chronic inflammation and protect the host [120,121].…”

Section: T Regulatory Cellsmentioning

confidence: 99%

“…During visceral leishmaniasis, IL-10 plays a crucial role in the immunosuppressive phase of the disease: high levels of this cytokine have been detected in patients with VL. It can lead to a fatal outcome in untreated cases of visceral leishmaniasis [118]. In this way, it appears Tregs may assist in parasite persistence by suppressing macrophage activation and helping the parasite evade the host immune response through the secretion of IL-10 and TGF-β, ultimately resulting in increased host susceptibility and parasite durability [118,126,127].…”

Section: T Regulatory Cellsmentioning

confidence: 99%

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Leishmaniasis: Immune Cells Crosstalk in Macrophage Polarization

Almeida¹,

Vanderley²,

Comberlang³

et al. 2023

Preprint

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Leishmaniasis is a complex infectious parasitic disease caused by protozoa of the genus Leishmania, belonging to a group of neglected tropical diseases. It poses significant global health challenges, particularly in socio-economically disadvantaged regions. Macrophages, as innate immune cells, play a crucial role in initiating the inflammatory response against the pathogens responsible for this disease. Macrophage polarization, the process of differentiating macrophages into pro-inflammatory (M1) or anti-inflammatory (M2) phenotypes, is essential for the immune response in leishmaniasis. The M1 phenotype is associated with resistance to Leishmania infection, while the M2 phenotype is predominant in susceptible environments. Notably, various immune cells, including T cells, play a significant role in modulating macrophage polarization by releasing cytokines that influence macrophage maturation and function. Furthermore, other immune cells can also impact macrophage polarization in a T-cell-dependent manner. Therefore, this review comprehensively examines macrophage polarization's role in leishmaniasis and other immune cells' potential involvement in this intricate process.

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Succinate coenzyme A ligase β‐like protein from Trichinella spiralis is a potential therapeutic molecule for allergic asthma

Aimulajiang,

Chu,

Liao

et al. 2024

Immunity Inflam & Disease

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BackgroundFor decades, studies have demonstrated the anti‐inflammatory potential of proteins secreted by helminths in allergies and asthma. Previous studies have demonstrated the immunomodulatory capabilities of Succinate Coenzyme A ligase beta‐like protein (SUCLA‐β) derived from Trichinella spiralis, a crucial excretory product of this parasite.ObjectiveTo explore the therapeutic potential of SUCLA‐β in alleviating and controlling ovalbumin (OVA)‐induced allergic asthma, as well as its influence on host immune modulation.MethodsIn this research, we utilized the rTs‐SUCLA‐β protein derived from T. spiralis to investigate its potential in mitigating airway inflammation in a murine model of asthma induced by OVA sensitization/stimulation, both pre‐ and post‐challenge. The treatment's efficacy was assessed by quantifying the extent of inflammation in the lungs.ResultsTreatment with rTs‐SUCLA‐β demonstrated efficacy in ameliorating OVA‐induced airway inflammation, as evidenced by a reduction in eosinophil infiltration, levels of OVA‐specific Immunoglobulin E, interferon‐γ, interleukin (IL)‐9, and IL‐17A, along with an elevation in IL‐10. The equilibrium between Th17 and Treg cells plays a pivotal role in modulating the abundance of inflammatory cells within the organism, thereby ameliorating inflammation and alleviating symptoms associated with allergic asthma.Conclusions and Clinical RelevanceOur data revealed that T. spiralis‐derived Ts‐SUCLA‐β protein may inhibit the allergic airway inflammation by regulating host immune responses.

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Role of Treg, Breg and other cytokine sets in host protection and immunopathology during human leishmaniasis: Are they potential valuable markers in clinical settings and vaccine evaluation?

Cited by 8 publications

References 45 publications

Leishmaniasis: Immune Cells Crosstalk in Macrophage Polarization

Leishmaniasis: Immune Cells Crosstalk in Macrophage Polarization

Leishmaniasis: Immune Cells Crosstalk in Macrophage Polarization

Succinate coenzyme A ligase β‐like protein from Trichinella spiralis is a potential therapeutic molecule for allergic asthma

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