IL-17 and related cytokines involved in systemic sclerosis: Perspectives

Gonçalves, Rafaela Silva Guimarães; Pereira, Michelly Cristiny; Dantas, Andréa Tavares; Almeida, Anderson Rodrigues de; Marques, Cláudia Diniz Lopes; Rego, MJ; Pitta, Ivan R.; Duarte, Ângela Luzia Branco Pinto; Pitta, M. G. R.

doi:10.1080/08916934.2017.1416467

Cited by 33 publications

(25 citation statements)

References 98 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Formation of aggregated NETs will be accompanied by the release of DNA-bound cytokine-degrading proteases [ 25 ] as well as enzymes degrading circulating immune complexes [ 41 ]. This makes the inflammation self-limiting.…”

Section: Resultsmentioning

confidence: 99%

Neutrophils as Main Players of Immune Response towards Nondegradable Nanoparticles

et al. 2020

View full text Add to dashboard Cite

Many nano/microparticles (n/µP), to which our body is exposed, have no physiological way of removal. Our immune system sense these “small particulate objects”, and tries to decrease their harmfulness. Since oxidation, phagocytosis and other methods of degradation do not work with small, chemically resistant, and hydrophobic nanoparticles (nP). This applies to soot from air pollution, nano-diamonds from cosmic impact, polishing and related machines, synthetic polymers, and dietary n/µP. Our body tries to separate these from the surrounding tissue using aggregates from neutrophil extracellular traps (NETs). This effectively works in soft tissues where n/µP are entrapped into granuloma-like structures and isolated. The interactions of hydrophobic nanocrystals with circulating or ductal patrolling neutrophils and the consequent formation of occlusive aggregated NETs (aggNETs) are prone to obstruct capillaries, bile ducts in gallbladder and liver, and many more tubular structures. This may cause serious health problems and often fatality. Here we describe how specific size and surface properties of n/µP can activate neutrophils and lead to aggregation-related pathologies. We discuss “natural” sources of n/µP and those tightly connected to unhealthy diets.

show abstract

Section: Resultsmentioning

confidence: 99%

Neutrophils as Main Players of Immune Response towards Nondegradable Nanoparticles

et al. 2020

View full text Add to dashboard Cite

show abstract

“…In vivo studies have shown that IL-17A-deficient mice were partially protected by bleomycin-induced scleroderma [30], and bleomycin-induced scleroderma was attenuated by anti-IL-17A antibody [31]. These results suggest that IL-17 is one of the main targets for treating SSc [32][33][34]. By contrast, a recent study has shown that IL-17 softens the skin through induction of matrix metalloproteinase-1(MMP-1) [35].…”

Section: Psoriasis and Sscmentioning

confidence: 99%

Psoriasis and Connective Tissue Diseases

Yamamoto

2020

IJMS

View full text Add to dashboard Cite

Psoriasis is a chronic systemic inflammatory disease with various co-morbidities, having been recently considered as a comprehensive disease named psoriatic disease or psoriatic syndrome. Autoimmune diseases are one form of its co-morbidities. In addition to the genetic background, shared pathogenesis including innate immunity, neutrophil extracellular trap (NETs), and type I interferon, as well as acquitted immunity such as T helper-17 (Th17) related cytokines are speculated to play a significant role in both psoriasis and connective tissue diseases. On the other hand, there are definite differences between psoriasis and connective tissue diseases, such as their pathomechanisms and response to drugs. Therefore, we cannot expect that one stone kills two birds, and thus caution is necessary when considering whether the administered drug for one disease is effective or not for another disease. In this review, several connective tissue diseases and related diseases are discussed from the viewpoint of their coexistence with psoriasis.

show abstract

“…One consequence of this immune deregulation is the alteration of T cell homeostasis, with an elevated frequency of Th17 cells in SSc patient peripheral blood and skin . Interleukin‐17 (IL‐17) is a cytokine involved in many pathologic features contributing to SSc pathology, including proinflammatory cytokine secretion, monocyte recruitment, and granulocyte–macrophage colony‐stimulating factor production .…”

Section: Introductionmentioning

confidence: 99%

Induction of Inflammation and Fibrosis by Semaphorin 4A in Systemic Sclerosis

Carvalheiro

Affandi

Malvar‐Fernández

et al. 2019

Arthritis & Rheumatology

View full text Add to dashboard Cite

Objective To analyze the potential role of semaphorin 4A (Sema4A) in inflammatory and fibrotic processes involved in the pathology of systemic sclerosis (SSc). Methods Sema4A levels in the plasma of healthy controls (n = 11) and SSc patients (n = 20) were determined by enzyme‐linked immunosorbent assay (ELISA). The expression of Sema4A and its receptors in monocytes and CD4+ T cells from healthy controls and SSc patients (n = 6–7 per group) was determined by ELISA and flow cytometry. Th17 cytokine production by CD4+ T cells (n = 5–7) was analyzed by ELISA and flow cytometry. The production of inflammatory mediators and extracellular matrix (ECM) components by dermal fibroblast cells (n = 6) was analyzed by quantitative polymerase chain reaction, ELISA, Western blotting, confocal microscopy, and ECM deposition assay. Results Plasma levels of Sema4A, and Sema4A expression by circulating monocytes and CD4+ T cells, were significantly higher in SSc patients than in healthy controls (P < 0.05). Inflammatory mediators significantly up‐regulated the secretion of Sema4A by monocytes and CD4+ T cells from SSc patients (P < 0.05 versus unstimulated SSc cells). Functional assays showed that Sema4A significantly enhanced the expression of Th17 cytokines induced by CD3/CD28 in total CD4+ T cells as well in different CD4+ T cell subsets (P < 0.05 versus unstimulated SSc cells). Finally, Sema4A induced a profibrotic phenotype in dermal fibroblasts from both healthy controls and SSc patients, which was abrogated by blocking or silencing the expression of Sema4A receptors. Conclusion Our findings indicate that Sema4A plays direct and dual roles in promoting inflammation and fibrosis, 2 main features of SSc, suggesting that Sema4A might be a novel therapeutic target in SSc.

show abstract

IL-17 and related cytokines involved in systemic sclerosis: Perspectives

Cited by 33 publications

References 98 publications

Neutrophils as Main Players of Immune Response towards Nondegradable Nanoparticles

Neutrophils as Main Players of Immune Response towards Nondegradable Nanoparticles

Psoriasis and Connective Tissue Diseases

Induction of Inflammation and Fibrosis by Semaphorin 4A in Systemic Sclerosis

Contact Info

Product

Resources

About