IL-23 (Interleukin-23)–Producing Conventional Dendritic Cells Control the Detrimental IL-17 (Interleukin-17) Response in Stroke

Gelderblom, Mathias; Gallizioli, Mattia; Ludewig, Peter; Thom, Vivien; Arunachalam, Priyadharshini; Rissiek, Björn; Bernreuther, Christian; Glatzel, Markus; Korn, Thomas; Arumugam, Thiruma V.; Sedlacik, Jan; Gerloff, Christian; Tolosa, Eva; Planas, Anna M.; Magnus, Tim

doi:10.1161/strokeaha.117.019101

Cited by 88 publications

(78 citation statements)

References 23 publications

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“…Interestingly, IL-23 deficient animals showed significantly lower levels of cdT cells, subsequent lower secretion of IL-17 and a decreased infarct size. 90 Similar results were obtained after inhibition of IL-12/IL-23p40 subunit. 93 Specific suppression of IL-23p19 subunit resulted in lower levels of proinflammatory IL-23 and IL-17 concurrent with upregulation of the Treg transcription factor FoxP3.…”

Section: Cerebrovascular Diseasesupporting

confidence: 68%

“…88,89 The importance of this pathway has been observed in several studies, which have shown elevations of the IL-23/IL-17 axis and IL-23R associated with worsening of neuron damage, compared with controls in animal stroke models. 86,87,90 In humans, increased levels of IL-23 along with a markedly increased proportion of IL-17A-producing cells and elevation of IL-17A levels, as well as other CKs, have been identified at several time points after stroke in comparison with controls. 91,92 Moreover, a positive correlation was found between IL-23 levels and lesion volume.…”

Section: Cerebrovascular Diseasementioning

confidence: 99%

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The role of the interleukin‐23/Th17 pathway in cardiometabolic comorbidity associated with psoriasis

Egeberg

Gisondi

Carrascosa

et al. 2020

Acad Dermatol Venereol

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Alterations in the innate and adaptive immunity underpin psoriasis pathophysiology, with the Th17 cells subset now recognized as the fundamental cells in the key controlling pathway involved in its pathogenesis. Since psoriasis is a systemic disease with important comorbidity, further knowledge on the interleukin (IL)-23/Th17 axis led to the hypothesis that there may be shared pathogenic pathways between primary skin disease and comorbidity. Psoriasis has been identified as a risk factor for cardiovascular and metabolic disease, and increasing evidence gives support to this epidemiological observation from the clinical-pathologically field. As an example, increased levels of IL-23 and IL-23R have been found in human atherosclerotic plaque, and levels correlated with symptom duration and mortality. Also, upregulation of IL-23/IL-17 seems to play an important role in both myocardial damage and stroke, with interesting reports on deleterious effect neutralization after administration of related anti-bodies in both associated conditions. In diabetic patients, increased levels of IL-23/IL-17 have also been observed and available data support a synergistic role of IL-23/IL-17 in b-cells damage. In obesity, signs of an expansion of Th17 subset in adipose tissue have been reported, as well as elevated concentrations of IL-23 in obese patients. In non-alcoholic fatty liver disease, closely related to metabolic syndrome, but also in other mentioned cardiometabolic disorders, a predominance of IL-23 and other related proinflammatory factors has been identified as participating in their pathogenesis. Thus, the involvement of the IL-23/Th17 axis in these shared psoriasis-cardiometabolic pathogenic mechanisms is reviewed and discussed in the light of the existing preclinical and clinical evidence, including that from comorbid psoriasis patients.

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Section: Cerebrovascular Diseasesupporting

confidence: 68%

Section: Cerebrovascular Diseasementioning

confidence: 99%

The role of the interleukin‐23/Th17 pathway in cardiometabolic comorbidity associated with psoriasis

Egeberg

Gisondi

Carrascosa

et al. 2020

Acad Dermatol Venereol

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“…After 24 h or 48 h of MCAO, mice were reanesthetized, and intracardiac perfusion with saline was performed. After removal, brains were placed in a brain matrice to obtain 1 mm thick coronal sections and were stained with 2,3,5-triphenyl-tetrazolium chloride solution (CAS 298-96-4; Loba Chemie) 61 . The stained sections were digitalized, and the infarct volume was determined using ImageJ.…”

Section: Discussionmentioning

confidence: 99%

Activation of GPR35 protects against cerebral ischemia by recruiting monocyte-derived macrophages

Sharmin

Abir

Potol

et al. 2020

Sci Rep

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after MCAO (Fig. 7B and Supplementary Fig. 1B) although the pAkt concentration was unaffected 48 h after the MCAO. Therefore, we conclude that activation of GPR35 on monocyte/macrophages by its ligand pamoic acid reprograms these cell types into neuroprotective pathways. Method Mice. Male Swiss albino mice (8-12 weeks) were collected from the North South University (NSU) animal house and were maintained under standard environmental conditions (temperature 23.0 ± 2.0 °C, relative humidity: 55-65% and 12 h light and dark cycle). All experiments were carried out according to the institutional guideline and were approved by the NSU Institutional Animal Care and Use Committee (IACUC).

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“…IL-17 has a specific role in the delayed phase of the ischemic brain injury inflammatory cascade (98). Shichita et al demonstrated that gdT17 cells play a significant role during latestage ischemic brain injury, and that they, rather Th17 cells, are (surprisingly) the major origin of IL-17 (99).…”

Section: Ischemic Brain Injurymentioning

confidence: 99%

The Role of Gamma-Delta T Cells in Diseases of the Central Nervous System

Zhang

et al. 2020

Front. Immunol.

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Gamma-delta (gd) T cells are a subset of T cells that promote the inflammatory responses of lymphoid and myeloid lineages, and are especially vital to the initial inflammatory and immune responses. Given the capability to connect crux inflammations of adaptive and innate immunity, gd T cells are responsive to multiple molecular cues and can acquire the capacity to induce various cytokines, such as GM-CSF, IL-4, IL-17, IL-21, IL-22, and IFN-g. Nevertheless, the exact mechanisms responsible for gd T cell proinflammatory functions remain poorly understood, particularly in the context of the central nervous system (CNS) diseases. CNS disease, usually leading to irreversible cognitive and physical disability, is becoming a worldwide public health problem. Here, we offer a review of the neuroinflammatory and immune functions of gd T cells, intending to understand their roles in CNS diseases, which may be crucial for the development of novel clinical applications.

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IL-23 (Interleukin-23)–Producing Conventional Dendritic Cells Control the Detrimental IL-17 (Interleukin-17) Response in Stroke

Abstract: Our results suggest a central role for interferon regulatory factor 4-positive IL-23-producing conventional DCs in the IL-17-dependent secondary tissue damage in stroke.

Cited by 88 publications

References 23 publications

The role of the interleukin‐23/Th17 pathway in cardiometabolic comorbidity associated with psoriasis

The role of the interleukin‐23/Th17 pathway in cardiometabolic comorbidity associated with psoriasis

Activation of GPR35 protects against cerebral ischemia by recruiting monocyte-derived macrophages

The Role of Gamma-Delta T Cells in Diseases of the Central Nervous System

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