CD1b-autoreactive T cells contribute to hyperlipidemia-induced skin inflammation in mice

Bagchi, Sreya; Hé, Ying; Zhao, Hong; Cao, Liang; Rhijn, Ildiko Van; Moody, D. Branch; Guðjónsson, Jóhann E.; Wang, Chyung Ru

doi:10.1172/jci92217

Cited by 54 publications

(61 citation statements)

References 59 publications

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“…Previous studies have shown that targeting inflammation might represent an alternative approach to suppress the hyperlipidemia and also the atherosclerosis [31,35,36]. Our data here demonstrated that IL-38, a newly identified anti-inflammatory factor, also showed protective effect during hyperlipidemia treatment in the clinic and alleviated atherosclerosis development in the mice model.…”

Section: Cellular Physiology and Biochemistrysupporting

confidence: 71%

Elevated Interleukin-38 Level Associates with Clinical Response to Atorvastatin in Patients with Hyperlipidemia

Yang

Song

Dong

et al. 2018

Cell Physiol Biochem

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Background/Aims: Hyperlipidemia is a risk factor for various cardiovascular and metabolic disorders. And it is tightly related to chronic inflammation. Interleukin-38 (IL-38) represents a new member of anti-inflammatory cytokines. Thus we studied the important role of IL-38 in hyperlipidemia development and treatment. Methods: The mRNA level of IL-38 in PBMCs (peripheral blood mononuclear cells) and serum IL-38 levels in hyperlipidemia patients and healthy controls were measured by real-time polymerase chain reaction (RT-PCR) and enzyme-linked immunoassay (ELISA). The hyperlipidemia patients were further divided into two groups (Sensitive and Resistant Group) according to their clinical response to Atorvastatin therapy. Finally, the effects of IL-38 on hyperlipidemia was evaluated in the mice model. Results: Data showed that the IL-38 mRNA and serum protein levels were higher in patients with hyperlipidemia compared with healthy controls. And the IL-38 mRNA and serum protein levels were higher in patients sensitive to Atorvastatin therapy than the resistant group. In vitro, IL-38 inhibited the production of IL-6, IL-1β and CRP in PBMCs of patients with hyperlipidemia. In the mice model of hyperlipidemia, IL-38 was also elevated during the hyperlipidemia development. Furthermore, the IL-38 over-expressed by adeno-associated virus significantly inhibited the hyperlipidemia development, inflammatory factor secretion and also the atherosclerosis process. Conclusion: Thus our data showed that IL-38 might present protective effects on hyperlipidemia treatment.

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Section: Cellular Physiology and Biochemistrysupporting

confidence: 71%

Elevated Interleukin-38 Level Associates with Clinical Response to Atorvastatin in Patients with Hyperlipidemia

Yang

Song

Dong

et al. 2018

Cell Physiol Biochem

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“…Lipid antigens can be presented on CD1 molecules and recognized by T cells (Figure 3). Frequency of both CD1b[20] and CD1a[21] autocreactive T cells is found to increase in psoriasis patients compared to healthy controls. Several phospholipases, including PLA2G4D and PLA2G2F, are increased in psoriatic skin[21,22], but these enzymes play a role in generation of phospholipid neoantigens.…”

Section: Genetics Adaptive Immune System and Evidence For Autoimmunimentioning

confidence: 99%

Psoriasis: a mixed autoimmune and autoinflammatory disease

Liang

Sarkar

Tsoi

et al. 2017

Current Opinion in Immunology

186

140

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In recent years marked progress has been made in our understanding of the critical biologic and immunologic pathways involved in psoriasis. Genetic studies have demonstrated that susceptibility to psoriasis involves components of both the adaptive and innate immune system and not surprisingly activation of both of these arms of the immune system is found in psoriatic skin. While adaptive immune responses predominate in chronic plaque psoriasis, innate and autoinflammatory responses dominate in pustular forms of psoriasis, with other clinical subtypes extending on a spectrum between plaque and pustular psoriasis. This makes psoriasis a unique disease where both autoimmune and autoinflammatory responses co-exist, with the balance between the two being critical in shaping its clinical presentation.

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“…Even more exciting has been the identification of specific immune cells, called CD1-restricted self-lipid-reactive T-cells in the blood or skin of humans [71], which may be the missing link between PsD and CVD. Furthermore, in a strain of mice with self-lipid-reactive T-cells and high levels of cholesterol, mice with hyperlipidemia began developing skin diseases mirroring the usual development of psoriasis in humans [72].…”

Section: Hyperlipidemiamentioning

confidence: 99%

Cardiovascular Comorbidities in Psoriatic Disease

Simonyi

Haroon²,

FitzGerald

2019

Rheumatol Ther

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Psoriatic disease (PsD) is a multisystem inflammatory disorder with a high prevalence of cardiovascular (CV) risk factors contributing to accelerated atherosclerosis and its sequelae. Imaging studies, notably with ultrasound, computed tomography, and positron emission tomography (PET) scanning have confirmed significant atherosclerotic change with plaque formation and vessel stenosis. Atherosclerosis is likely driven by a combination of traditional risk factors which occur more frequently in PsD and by systemic inflammation with associated pro-inflammatory cytokine production. While the mechanisms driving atherosclerosis in PsD are incompletely understood, it is now best practice to try to minimize the impact of CV risk factors by regular assessment, prevention, and treatment and also by ensuring that inflammatory musculoskeletal and cutaneous disease is adequately suppressed. Future studies need to focus on improving our understanding of the mechanisms driving atherosclerosis and, as a consequence, developing more rationale approaches to prevention and treatment.

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CD1b-autoreactive T cells contribute to hyperlipidemia-induced skin inflammation in mice

Cited by 54 publications

References 59 publications

Elevated Interleukin-38 Level Associates with Clinical Response to Atorvastatin in Patients with Hyperlipidemia

Elevated Interleukin-38 Level Associates with Clinical Response to Atorvastatin in Patients with Hyperlipidemia

Psoriasis: a mixed autoimmune and autoinflammatory disease

Cardiovascular Comorbidities in Psoriatic Disease

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