Research Area: Inflammatory & autoimmune disease
Development Stage: Optimization
Goal: Identify differences in mechanism for Multiple Sclerosis patients in response to novel therapeutics, such as TLR2 therapy
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Identification of enhanced MS response to TLR2 stimulation through IsoPlexis’ PSI. CD14+ monocyte PSI was calculated for control (n=8) and MS patient samples (n=8) stimulated for 24 hours with P3C (TLR2 stimulation). The PSI of the MS patients samples was notably higher than in the control samples; the PSI of both sample groups was dominated by polyfunctional IL-8 secretions.
Statistical analysis showed that the PSI of the MS patients (mean = 34) are statistically higher (p = 0.0348) than the PSI of the control samples (mean = 14). The level of PSI representing the upper threshold of control responses (based on the control IQR) is depicted by the dashed line. The percent of responses above threshold is depicted for controls and total MS patients. The difference in PSI between the two groups suggests an important role of TLR2 signaling in mediating MS disease progress.1
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In vitro single CD14+ MO PSI differences between MS patient groups with no treatment, versus treated with Tysabri. LPS-stimulated samples show significant upregulation in polyfunctional cytokine signal between untreated MS patients (n=6) and Tysabri treated MS patients (n=3).
Activated CD14+CD16+ MO cells are thought to be one of the first immune cells to initiate and promote brain inflammation contributing to the disease progression of MS.1