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Treatment of granuloma annulare and suppression of pro-inflammatory cytokine activity with tofacitinib

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE158926 | GEO | 2020/12/22

REPOSITORIES: GEO

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Treatment of granuloma annulare and suppression of pro-inflammatory cytokine activity with tofacitinib [scRNA-Seq]

Project description:Granuloma annulare (GA) is a common inflammatory cutaneous disorder characterized by macrophage accumulation and activation in the skin. Its pathogenesis is poorly understood and there are no reliably effective treatments. Its potential health implications, if any, are unknown. Using single cell RNA sequencing (scRNAseq) we show that in GA, CD4+ T cells over-produce interferon (IFN)-g resulting in inflammatory polarization of macrophages and in altered extracellular matrix (ECM) production induced by the activity of oncostatin M, an interleukin (IL)-6 family cytokine, on fibroblasts. This mechanism identifies Janus kinase (JAK) inhibition as a potential therapeutic strategy, as both IFN-g and OSM signal via the JAK-STAT pathway. Indeed, treatment of five patients with severe, longstanding GA with tofacitinib (a JAK1/3 inhibitor) resulted in clinical and histologic disease remission in three patients and marked improvement in the other two. Treatment was associated with suppression of pathogenic cytokine activity in the skin and dissolution of macrophages. We also found that severe GA was associated with hypercytokinemia in plasma of patients, and JAK inhibition normalized this hypercytokiemia. Together, our results highlight the constitutive activity of the JAK-STAT pathway in GA as a result of IFN-g and OSM and identify JAK inhibitors as a potential molecularly targeted treatment for this disorder.

2020-12-22 | GSE158924 | GEO

Treatment of granuloma annulare and suppression of pro-inflammatory cytokine activity with tofacitinib [RNA-Seq]

2020-12-22 | GSE158923 | GEO

Treatment of granuloma annulare and suppression of pro-inflammatory cytokine activity with tofacitinib

Project description:Treatment of granuloma annulare and suppression of pro-inflammatory cytokine activity with tofacitinib

| PRJNA667031 | ENA

Treatment of granuloma annulare and suppression of pro-inflammatory cytokine activity with tofacitinib [scRNA-Seq]

Project description:Treatment of granuloma annulare and suppression of pro-inflammatory cytokine activity with tofacitinib [scRNA-Seq]

| PRJNA667044 | ENA

Treatment of granuloma annulare and suppression of pro-inflammatory cytokine activity with tofacitinib [RNA-Seq]

Project description:Treatment of granuloma annulare and suppression of pro-inflammatory cytokine activity with tofacitinib [RNA-Seq]

| PRJNA667045 | ENA

Pro-inflammatory cytokine treatments in primary mouse hepatocytes

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-10-10 | GSE96770 | GEO

Selective suppression of endothelial cytokine production by progesterone receptor

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-01-01 | E-GEOD-46503 | biostudies-arrayexpress

A role for miR-4734 in conditional suppression of ER stress-associated pro-inflammatory responses

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-10-10 | GSE214963 | GEO

Early quantification of systemic inflammatory (INF) and cardiovascular disease (CVD) proteins predicts long-term treatment response to Tofacitinib and Etanercept

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-11-22 | GSE136435 | GEO

The Pro-inflammatory Cytokine Interleukin-1β is a Key Regulatory Factor for the Postictal Suppression in Mice.

Project description:AimsThe postictal suppression (PS) is a common and important period following an epileptic seizure but has not been well studied. This study was designed to determine whether interleukin-1β (IL-1β) is involved in the PS.MethodsThe effects of IL-1β on the PS were tested in three independent seizure models induced by hippocampal kindling, maximal electroshock seizure (MES), and 4-aminopyridine, respectively.ResultsIL-1R1 knockout or IL-1RA enhanced the seizure refractory phenomenon without influencing the baseline seizure threshold in intermittent MES model. IL-1β attenuated the seizure refractory phenomenon without affecting the severity of the preceding seizures in hippocampal kindling model, while IL-1RA enhanced it. Besides, IL-1β reduced the postictal EEG suppression period, while IL-1RA prolonged it. And IL-1β showed no further effect on the postictal EEG suppression and seizure refractory phenomenon in IL-1R1 knockout mice. In addition, 30 min after intrahippocampal injection of 4-aminopyridine, IL-1β increased the incidence of SE, while IL-1RA prolonged the intervals between recurrent seizures.ConclusionsThis study provides the first direct evidence that IL-1β is key regulatory factor for the PS, and its receptor IL-1R1 may be a potential target for adjuvant treatment of postictal problems.

| S-EPMC6495150 | biostudies-literature

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