About InVivoSIM anti-human IL-17A (Secukinumab Biosimilar) This non-therapeutic biosimilar antibody uses the same variable regions from the therapeutic antibody Secukinumab making it ideal for research use. This Secukinumab biosimilar reacts with human IL-17A, a 15-20 kDa cytokine expressed by Th17 cells, γδ T cells, iNKT cells, NK cells, LTi cells, neutrophils, and intestinal Paneth cells. IL-17A has pleiotropic effects in immunoregulation and inflammation. It plays an important role in anti-microbial and chronic inflammation by inducing cytokine and chemokine production, neutrophil influx, and the production of antibacterial peptides but it is also an inflammatory mediator in the development of autoimmune diseases including rheumatoid arthritis, asthma, multiple sclerosis, and psoriasis. Secukinumab neutralizes IL-17A. InVivoSIM anti-human IL-17A (Secukinumab Biosimilar) Specifications IsotypeHuman IgG1 Recommended Isotype Control(s)RecombiMAb human IgG1 isotype control, anti-hen egg lysozyme Recommended Dilution BufferInVivoPure pH 7.0 Dilution Buffer ImmunogenHuman IL-17A Reported Applicationsin vitro IL-17A neutralization Functional assays Immunofluorescence Immunohistochemistry Flow Cytometry ELISA FormulationPBS, pH 7.0 Contains no stabilizers or preservatives Endotoxin<0.5EU/mg (<0.0005EU/μg) Determined by LAL gel clotting assay Aggregation<5% Determined by SEC Purity>95% Determined by SDS-PAGE Sterility0.2 μm filtration ProductionPurified from cell culture supernatant in an animal-free facility PurificationProtein A RRIDAB_2894734 Molecular Weight150 kDa StorageThe antibody solution should be stored at the stock concentration at 4°C. Do not freeze. Application ReferencesInVivoSIM anti-human IL-17A (Secukinumab Biosimilar) (CLONE: Secukinumab)Wang F, Li Y, Yang Z, Cao W, Liu Y, Zhao L, Zhang T, Zhao C, Yu J, Yu J, Zhou J, Zhang X, Li PP, Han M, Feng S, Ng BW, Hu ZW, Jiang E, Li K, Cui B (2024). "Targeting IL-17A enhances imatinib efficacy in Philadelphia chromosome-positive B-cell acute lymphoblastic leukemia" Nat Commun 15(1):203. PubMedDysregulated hematopoietic niches remodeled by leukemia cells lead to imbalances in immunological mediators that support leukemogenesis and drug resistance. Targeting immune niches may ameliorate disease progression and tyrosine kinase inhibitor (TKI) resistance in Philadelphia chromosome-positive B-ALL (Ph+ B-ALL). Here, we show that T helper type 17 (Th17) cells and IL-17A expression are distinctively elevated in Ph+ B-ALL patients. IL-17A promotes the progression of Ph+ B-ALL. Mechanistically, IL-17A activates BCR-ABL, IL6/JAK/STAT3, and NF-kB signalling pathways in Ph+ B-ALL cells, resulting in robust cell proliferation and survival. In addition, IL-17A-activated Ph+ B-ALL cells secrete the chemokine CXCL16, which in turn promotes Th17 differentiation, attracts Th17 cells and forms a positive feedback loop supporting leukemia progression. These data demonstrate an involvement of Th17 cells in Ph+ B-ALL progression and suggest potential therapeutic options for Ph+ B-ALL with Th17-enriched niches.
