Human EBI3(Interleukin-27 subunit beta) ELISA Kit

Autoreactive CD4(+) T-cells are considered to play a major role in the pathogenesis of multiple sclerosis. In experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis, exogenous and endogenous type I interferons restrict disease severity. Recombinant interferon-beta is used for treatment of multiple sclerosis, and some untreated multiple sclerosis patients have increased expression levels of type I interferon-inducible genes in immune cells. The role of endogenous type I interferons in multiple sclerosis is controversial: some studies found an association of high expression levels of interferon-beta-inducible genes with an increased expression of interleukin-10 and a milder disease course in untreated multiple sclerosis patients, whereas other studies reported an association with a poor response to treatment with interferon-beta. In the present study, we found that untreated multiple sclerosis patients with an increased expression of interferon-beta-inducible genes in peripheral blood mononuclear cells and interferon-beta-treated multiple sclerosis patients had decreased CD4(+) T-cell reactivity to the autoantigen myelin basic protein ex vivo. Interferon-beta-treated multiple sclerosis patients had increased IL10 and IL27 gene expression levels in monocytes in vivo. In vitro, neutralization of interleukin-10 and monocyte depletion increased CD4(+) T-cell reactivity to myelin basic protein while interleukin-10, in the presence or absence of monocytes, inhibited CD4(+) T-cell reactivity to myelin basic protein. Our findings suggest that spontaneous expression of interferon-beta-inducible genes in peripheral blood mononuclear cells from untreated multiple sclerosis patients and treatment with interferon-beta are associated with reduced myelin basic protein-induced T-cell responses. Reduced myelin basic protein-induced CD4(+) T-cell autoreactivity in interferon-beta-treated multiple sclerosis patients may be mediated by monocyte-derived interleukin-10.

Human papillomavirus (HPV) is recommended as the primary test in cervical cancer screening, with co-testing by cytology for HPV-positive women to identify cervical lesions. Cytology has low sensitivity and there is a need to identify biomarkers that could identify dysplasia that are likely to progress to cancer. We searched for plasma proteins that could identify women with cervical cancer using the multiplex proximity extension assay (PEA). The abundance of 100 proteins were measured in plasma collected at the time of diagnosis of patients with invasive cervical cancer and in population controls using the Olink Multiplex panels CVD II, INF I, and ONC II. Eighty proteins showed increased levels in cases compared with controls. We identified a signature of 11 proteins (PTX3, ITGB1BP2, AXIN1, STAMPB, SRC, SIRT2, 4E-BP1, PAPPA, HB-EGF, NEMO and IL27) that distinguished cases and controls with a sensitivity of 0.96 at a specificity of 1.0. This signature was evaluated in a prospective replication cohort with samples collected before, at or after diagnosis and achieved a sensitivity of 0.78 and a specificity 0.56 separating samples collected at the time of diagnosis of invasive cancer from samples collected prior to diagnosis. No difference in abundance was seen between samples collected prior to diagnosis or after treatment as compared with population controls, indicating that this protein signature is mainly informative close to time of diagnosis. Further studies are needed to determine the optimal window in time prior to diagnosis for these biomarker candidates.