The Double Game Played by Th17 Cells in Infection: Host Defense and Immunopathology

Paroli, Marino; Caccavale, Rosalba; Fiorillo, Maria Teresa; Spadea, Luca; Gumina, Stefano; Candela, Vittorio; Paroli, Maria Pia

doi:10.3390/pathogens11121547

Cited by 27 publications

(15 citation statements)

References 177 publications

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“…In addition to their defensive action against pathogens, members of the IL-17 family can exacerbate tissue injury, because of their pro-inflammatory activity. IL-17 induces neutrophil recruitment, activation of the innate immune system, and enhancement of B-lymphocyte functions [ 48 ]. It has been reported that IL-17 levels correlate with SLEDAI in patients with LN [ 49 , 50 ].…”

Section: Sle Pathogenesismentioning

confidence: 99%

Advances in the Pathogenesis and Treatment of Systemic Lupus Erythematosus

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Caccavale

Paroli

et al. 2023

IJMS

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Systemic lupus erythematosus (SLE) is a genetically predisposed, female-predominant disease, characterized by multiple organ damage, that in its most severe forms can be life-threatening. The pathogenesis of SLE is complex and involves cells of both innate and adaptive immunity. The distinguishing feature of SLE is the production of autoantibodies, with the formation of immune complexes that precipitate at the vascular level, causing organ damage. Although progress in understanding the pathogenesis of SLE has been slower than in other rheumatic diseases, new knowledge has recently led to the development of effective targeted therapies, that hold out hope for personalized therapy. However, the new drugs available to date are still an adjunct to conventional therapy, which is known to be toxic in the short and long term. The purpose of this review is to summarize recent advances in understanding the pathogenesis of the disease and discuss the results obtained from the use of new targeted drugs, with a look at future therapies that may be used in the absence of the current standard of care or may even cure this serious systemic autoimmune disease.

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Section: Sle Pathogenesismentioning

confidence: 99%

Advances in the Pathogenesis and Treatment of Systemic Lupus Erythematosus

Accapezzato

Caccavale

Paroli

et al. 2023

IJMS

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“…It has also been observed that nasal colonization with S. aureus is often present in GPA, especially in relapsing patients. It has been suggested that this pathogen might contribute to an inflammatory microenvironment necessary for the activation of autoreactive T cells in AAV [ 70 , 71 ]. The direct pathogenicity of ANCA is supported by both experimental and clinical observations [ 72 , 73 ].…”

Section: Pathogenesismentioning

confidence: 99%

New Insights into Pathogenesis and Treatment of ANCA-Associated Vasculitis: Autoantibodies and Beyond

2023

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Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis is a group of rare systemic diseases affecting small-caliber vessels. The damage caused by AAV mainly involves the lung and kidneys. AAV includes three different types: granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA), and eosinophilic granulomatosis with polyangiitis (EGPA). Although the different phenotypic forms of AAV share common features, recent studies have shown that there are significant differences in terms of pathogenetic mechanisms involving both the adaptive and innate immune systems. Advances in our understanding of pathogenesis have enabled the development of immuno-targeted therapies. This review illustrates the characteristics of the various forms of AAV and the new therapies available for this disease that can have lethal consequences if left untreated.

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“…In addition, introducing the IRAK4 kinase dead in knock-in mice was shown to cause resistance to the induction and progression of Th17-cells driven experimental autoimmune encephalomyelitis [ 76 ]. It is worth mentioning that Th17-cells are considered as key pathogenic T cells involved in multiple inflammatory and autoimmune diseases [ 77 ]. Also, lupus-prone mice harboring the kinase-inactive IRAK4 showed reduced glomerulonephritis, splenomegaly, serum anti-nuclear antibodies and lower TNF-α expression in macrophages compared with lupus-prone mice with functional IRAK4 [ 74 ].…”

Section: Irak4mentioning

confidence: 99%

Modulation of IRAK enzymes as a therapeutic strategy against SARS-CoV-2 induced cytokine storm

2023

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of the current pandemic coronavirus disease 2019 (COVID-19). Dysregulated and excessive production of cytokines and chemokines, known as cytokine storm, is frequently seen in patients with severe COVID-19 disease and it can provoke a severe systematic inflammation in the patients. The IL-1R/TLRs/IRAKs signaling network is a key pathway in immune cells that plays a central role in regulating innate immunity and inflammatory responses via stimulating the expression and production of various proinflammatory molecules including cytokines. Modulation of IRAKs activity has been proposed to be a promising strategy in the treatment of inflammatory disorders. In this review, we highlight the biochemical properties of IRAKs and their role in regulating inflammatory molecular signaling pathways and discuss the potential targeting of IRAKs to suppress the SARS-CoV-2-induced cytokine storm in COVID-19 patients.

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The Double Game Played by Th17 Cells in Infection: Host Defense and Immunopathology

Cited by 27 publications

References 177 publications

Advances in the Pathogenesis and Treatment of Systemic Lupus Erythematosus

Advances in the Pathogenesis and Treatment of Systemic Lupus Erythematosus

New Insights into Pathogenesis and Treatment of ANCA-Associated Vasculitis: Autoantibodies and Beyond

Modulation of IRAK enzymes as a therapeutic strategy against SARS-CoV-2 induced cytokine storm

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