Search results for "Interleukin 17"
showing 5 items of 75 documents
Role of the IL-23/IL-17 Pathway in Rheumatic Diseases: An Overview
2021
Interleukin-23 (IL-23) is a pro-inflammatory cytokine composed of two subunits, IL-23A (p19) and IL-12/23B (p40), the latter shared with Interleukin-12 (IL-12). IL-23 is mainly produced by macrophages and dendritic cells, in response to exogenous or endogenous signals, and drives the differentiation and activation of T helper 17 (Th17) cells with subsequent production of IL-17A, IL-17F, IL-6, IL-22, and tumor necrosis factor α (TNF-α). Although IL-23 plays a pivotal role in the protective immune response to bacterial and fungal infections, its dysregulation has been shown to exacerbate chronic immune-mediated inflammation. Well-established experimental data support the concept that IL-23/IL…
Tumor-Infiltrating γδ T Lymphocytes: Pathogenic Role, Clinical Significance, and Differential Programing in the Tumor Microenvironment.
2014
There is increasing clinical evidence indicating that the immune system may either promote or inhibit tumor progression. Several studies have demonstrated that tumors undergoing remission are largely infiltrated by T lymphocytes [tumor-infiltrating lymphocytes (TILs)], but on the other hand, several studies have shown that tumors may be infiltrated by TILs endowed with suppressive features, suggesting that TILs are rather associated with tumor progression and unfavorable prognosis. γδ T lymphocytes are an important component of TILs that may contribute to tumor immunosurveillance, as also suggested by promising reports from several small phase-I clinical trials. Typically, γδ T lymphocytes …
A10.18 Lack of Association of Serum Interleukin-17 and Interleukin-23 Levels with Disease Activity in Patients with Ankylosing Spondylitis in Latvia
2013
Background Ankylosing spondylitis (AS) is a clinically well-known chronic inflammatory disease of the axial skeleton and peripheral joints. The pathogenesis of this disease still remains a challenge. Determination of cytokine profile and its role involved in AS pathogenesis give an opportunity to extend the targeted therapeutic approach. Interleukin-17 (IL-17) and interleukin-23 (IL-23) are cytokines of interest in the investigation of the pathogenesis of spondyloarthritides although their importance in AS is not clearly defined. Objectives to investigate levels of IL-17 and IL-23 in a group of AS and in a demographically matched group of healthy subjects and its association with the diseas…
A Case of Moderate Hidradenitis Suppurativa and Psoriasis Treated with Secukinumab
2018
Hidradenitis suppurativa (HS) is a disorder of the apocrine gland causing a chronic, recurrent and painful inflammation. It is a disabilitating condition and, though many therapeutic options are available, the response is often ineffective in most cases and patients can present many recurrences with physical and psychological sequelae. Recent data had shown increased interleukin (IL)-17 serum levels in patients with HS. Psoriasis is a chronic immune-mediated inflammatory disorder and new evidences have shown the role of Th17 cells in its pathogenesis and the therapeutic efficacy of anti-IL-17 antibodies. We present a case of a patient suffering from psoriasis and HS successfully treated wit…
Detection of natural killer T cells in mice infected with Rickettsia conorii.
2013
Little information is available regarding the role of natural killer T (NKT) cells during the early stage of Rickettsia conorii infection. Herein, C3H/HeN mice were infected with the Malish 7 strain of R. conorii. Splenocytes from these mice were analysed in the early stage of the infection by flow cytometry and compared with uninfected controls. Our results showed an increase in NKT cells in infected mice. Additionally, NKT interleukin (IL)-17(+) cells increased three days after infection, together with a concurrent decrease in the relative amount of NKT interferon (IFN)-γ(+) cells. We also confirmed a higher amount of NK IFN-γ(+) cells in infected mice. Taken together, our data showed tha…