IL-17/IL-23 biAb / BMS - LARVOL DELTA

Biologics Targeting the IL-23/IL-17 Pathway in Psoriatic Disease: Treating Beyond the Skin (Medscape)

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[VIRTUAL] PROTEOMICS ANALYSIS COMPARING THE MODE OF ACTION OF UPADACITINIB BETWEEN NON-BIOLOGIC-DMARD-IR AND BIOLOGIC-DMARD-IR PsA PATIENTS IDENTIFIES DISTINCT PATHOGENIC PATHWAYS IN THE SELECT-PsA 1 AND SELECT-PsA 2 PHASE 3 STUDIES (EULAR 2021) - "However, analysis of pBMs differentially modulated by UPA in R vs NR indicated that favorable clinical response (achievement of ACR50, PASDAS MDA, and PASI75) in DMARD-IR patients was associated with the down modulation of pBMs predicted to be linked to IFN, IL10, IL17, IL22, and IL27 pathways; while favorable clinical response in bio-IR patients was associated with the down modulation of multiple pBM predicted to be linked to the IL17, IL23, and IL1 pathways. UPA effects in both DMARD-IR and bio-IR PsA patients likely stem from the direct and indirect inhibition of multiple biological pathways belonging to the adaptive and innate immune systems. Responder/Non-Responder analysis suggests a possible shift from a TH1 biased biology in DMARD-IR PsA patients to a more TH17 biased biology in bio-IR PsA patients. This apparent change in the disease biology of PsA patients after inadequate response to prior therapy could be attributed to the actual alteration of the disease..."

Clinical • P3 data • Immunology • Inflammation • Musculoskeletal Diseases • IL10 • IL17A • IL22 • IL6 • JAK1

FABP4 facilitates inflammasome activation to induce the Treg/Th17 imbalance in preeclampsia via forming a positive feedback with IL-17A. (PubMed, Mol Ther Nucleic Acids) - "Overexpression of FABP4 promoted Th17 differentiation via increasing IL-17A/IL-23 release...The in vivo studies revealed that FABP4 inhibitor BMS309403 ameliorated PE clinical phenotypes, the Treg/Th17 imbalance, and NLRP3 inflammasome activation in PE mice model. In conclusion, FABP4 facilitates inflammasome activation to induce the imbalance of Treg/Th17 in PE via forming a positive feedback with IL-17A."

Journal • Gynecology • FABP4 • IL17A

The immunosuppressive tumor microenvironment (TME) in nasopharyngeal carcinoma: implications for immunotherapy (AACR 2018) - "...Compared to 12 EBV+ Hodgkin lymphomas (Duffield, Blood Advances 2017), EBV+ NPCs demonstrated a Th17 cytokine profile with overexpression of IL1A, IL17RC, IL23A, and IL23R...While these findings should be explored in a larger cohort, they have potential implications for designing combination NPC treatment regimens with anti-PD-1, which might include inhibitors of LAG-3, IDO, IL-17/-23, COX2, and/or IL-8. Funded by the Bristol-Myers Squibb International Immuno-Oncology Network and NCI R01 CA142779"

Biomarker • IO Biomarker • PD(L)-1 Biomarker • Tumor microenvironment • Hodgkin Lymphoma

Characterization of burning mouth syndrome profiles based on response to a local anaesthetic lozenge. (PubMed, Oral Dis) - "Our findings indicate that the response to treatment with local anaesthesia enables subgrouping of patients with BMS according to the potential pathogenic mechanisms. Effect of local anaesthesia indicates a peripheral neuropathology involving lack of oestrogen and upregulation of oestrogen receptors, and no effect indicates a systemic inflammation-induced mechanism leading to increased levels of plasma cytokines."

Journal • Anesthesia • Immunology • Pain

Immunoregulation of Bone Marrow-Derived Mesenchymal Stem Cells on the Chronic Cigarette Smoking-Induced Lung Inflammation in Rats. (PubMed) - Biomed Res Int - "Transfusion of BMSCs limited chronic smoking-related reduction in the levels of serum and lung iNOS and mitigated smoking-induced STAT5 phosphorylation in lymphocytes from lung tissue. BMSCs negatively regulated smoking-induced autoimmune responses in the lungs of rats and may be promising for the intervention of chronic smoking-related lung injury."

Journal • Biosimilar • Immunology • Inflammation

MM-BMSCs induce naïve CD4+ T lymphocytes dysfunction through fibroblast activation protein α. (PubMed, Oncotarget) - "MM-BMSCs inhibit T-cell proliferation and drive Th17 differentiation through FAPα/TGF-β axis, leading to the progression of myeloma. FAPα-induced T-cell senescence is mediated by the PI3K signaling pathway."

Journal • Biosimilar • Hematological Malignancies • Multiple Myeloma • Oncology