Increased expression of IL-1R8 and a possible immunomodulatory role of its ligand IL-37 in allergic rhinitis patients

Li, Cong; Shen, Yang; Wang, Jue; Ma, Zuxia; Xia, Ke; Wang, Zhihai; Hong, Suling; Hu, Guohua

doi:10.1016/j.intimp.2018.04.002

Cited by 7 publications

(6 citation statements)

References 17 publications

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“…Directly stimulating aged T‐cells with rIL‐37 also augmented the expression levels of genes which promote interferon production (IFN‐γ, TBK1, and IRF3), coincident with increased IFN‐γ production from aged T‐cells after αCD3/αCD28 stimulation. Our observations support recent studies demonstrating that IL‐37 treatment restores normal T‐cell function (reduction in IL‐17 production) in the chronic inflammatory setting of allergic rhinitis (Li, Shen, et al, 2018).…”

Section: Discussionsupporting

confidence: 91%

Interleukin‐37 improves T‐cell‐mediated immunity and chimeric antigen receptor T‐cell therapy in aged backgrounds

et al. 2021

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Aging‐associated declines in innate and adaptive immune responses are well documented and pose a risk for the growing aging population, which is predicted to comprise greater than 40 percent of the world's population by 2050. Efforts have been made to improve immunity in aged populations; however, safe and effective protocols to accomplish this goal have not been universally established. Aging‐associated chronic inflammation is postulated to compromise immunity in aged mice and humans. Interleukin‐37 (IL‐37) is a potent anti‐inflammatory cytokine, and we present data demonstrating that IL‐37 gene expression levels in human monocytes significantly decline with age. Furthermore, we demonstrate that transgenic expression of interleukin‐37 (IL‐37) in aged mice reduces or prevents aging‐associated chronic inflammation, splenomegaly, and accumulation of myeloid cells (macrophages and dendritic cells) in the bone marrow and spleen. Additionally, we show that IL‐37 expression decreases the surface expression of programmed cell death protein 1 (PD‐1) and augments cytokine production from aged T‐cells. Improved T‐cell function coincided with a youthful restoration of Pdcd1, Lat, and Stat4 gene expression levels in CD4+ T‐cells and Lat in CD8+ T‐cells when aged mice were treated with recombinant IL‐37 (rIL‐37) but not control immunoglobin (Control Ig). Importantly, IL‐37‐mediated rejuvenation of aged endogenous T‐cells was also observed in aged chimeric antigen receptor (CAR) T‐cells, where improved function significantly extended the survival of mice transplanted with leukemia cells. Collectively, these data demonstrate the potency of IL‐37 in boosting the function of aged T‐cells and highlight its therapeutic potential to overcome aging‐associated immunosenescence.

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Section: Discussionsupporting

confidence: 91%

Interleukin‐37 improves T‐cell‐mediated immunity and chimeric antigen receptor T‐cell therapy in aged backgrounds

et al. 2021

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“…Although the levels of IL-4, IL-13 and IL-17 were significantly reduced by IL-37, similar to the results reported in previous studies (14,16,24,39), the mechanism of IL-37 in the regulation of cytokines has yet to be determined. CCL11 is critical for the attraction of eosinophils during allergic asthma.…”

Section: Discussionsupporting

confidence: 78%

“…IL-37 is a unique member of the IL-1 family with broad anti-inflammatory roles during autoimmune diseases, including systemic lupus erythematosus, psoriasis and asthma (11)(12)(13). Several studies have reported that IL-37 alleviates allergic inflammation during AR (14)(15)(16). In animal models, administration of recombinant human IL-37 may attenuate the local allergic symptoms of AR and decrease the expression of cytokines produced by Th2 and Th17 cells in the nasal mucosa (15).…”

Section: Introductionmentioning

confidence: 99%

“…In animal models, administration of recombinant human IL-37 may attenuate the local allergic symptoms of AR and decrease the expression of cytokines produced by Th2 and Th17 cells in the nasal mucosa (15). IL-37 has also been demonstrated to regulate aberrant T-cell immune responses in patients with AR (16).…”

Section: Introductionmentioning

confidence: 99%

“…Wang et al (14) reported that phosphorylation of STAT proteins, together with IL-37 signaling and exogenous IL-37 treatment, is able to attenuate allergic symptoms (nasal rubbing and sneezing) by decreasing STAT6 or STAT3 expression levels in CD4 + T-cell subsets (14). The increased expression of IL-1R8 in CD4 + T cells may be associated with the potential role of IL-37 during AR-mediated anti-inflammation (16). Further studies have focused on the role of IL-37 in limiting innate inflammation primarily by inhibiting the production of proinflammatory cytokines by macrophages or epithelial cells (17,18).…”

Section: Introductionmentioning

confidence: 99%

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IL‑37 relieves allergic inflammation by inhibiting the CCL11 signaling pathway in a mouse model of allergic rhinitis

2020

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Allergic rhinitis (AR) is the allergic inflammation of immune cells in the nasal mucosa, caused by an abnormal T-cell response. Interleukin (IL)-37, a unique member of the IL-1 family with broad anti-inflammatory roles in various autoimmune diseases, participates in the immune regulation of AR. However, the regulatory mechanism of IL-37 in AR has remained elusive. In the present study, a mouse model of AR was established by treating mice with ovalbumin (OVA). Following systemic administration of IL-37, the effects of the cytokine on allergic symptoms were evaluated. The nasal mucosal infiltration of eosinophils was assessed by histopathological observation. The serum and nasal lavage fluid concentrations of immunoglobulin (Ig)E, IgG1, IgG2a, interferon (IFN)-γ, IL-4, IL-13, IL-17a and CC motif cytokine ligand (CCL)11 were determined by ELISA. Treatment with OVA resulted in allergic symptoms, including enhanced eosinophil infiltration in the nasal mucosa, increased thickness of the nasal mucosa and increased levels of IgE, IgG1, IgG2a, IL-4, IL-13, IL-17a and CCL11, but the level of IFN-γ was indicated to decrease. After IL-37 treatment, the frequency of nasal rubbing and sneezing was reduced compared with that in the OVA group. IL-37 administration also decreased the number of eosinophils in the nasal mucosa and the thickness of the nasal mucosa, as well as the serum and nasal lavage fluid levels of IgE, IgG1, IgG2a, IL-4, IL-13, IL-17a and CCL11, but the level of IFN-γ decreased. In addition, the OVA-induced increases in histamine and substance P levels were reversed by IL-37 administration. CCL11 expression levels were correlated with the expression levels of IFN-γ, IL-4, IL-13, IL-17a, histamine and substance P. In conclusion, IL-37 alleviated the OVA-induced allergic symptoms and allergic inflammatory response by reducing the serum cytokine levels via decreasing CCL11 expression levels in mice.

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The Role of New IL-1 Family Members (IL-36 and IL-38) in Atopic Dermatitis, Allergic Asthma, and Allergic Rhinitis

Tsang

Sun

Wong

2020

Curr Allergy Asthma Rep

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Increased expression of IL-1R8 and a possible immunomodulatory role of its ligand IL-37 in allergic rhinitis patients

Cited by 7 publications

References 17 publications

Interleukin‐37 improves T‐cell‐mediated immunity and chimeric antigen receptor T‐cell therapy in aged backgrounds

Interleukin‐37 improves T‐cell‐mediated immunity and chimeric antigen receptor T‐cell therapy in aged backgrounds

IL‑37 relieves allergic inflammation by inhibiting the CCL11 signaling pathway in a mouse model of allergic rhinitis

The Role of New IL-1 Family Members (IL-36 and IL-38) in Atopic Dermatitis, Allergic Asthma, and Allergic Rhinitis

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