rat il-17 elisa kit ebioscience 88-7170  (Thermo Fisher)

Journal: bioRxiv

Article Title: Postpartum cytokine shifts and IL-10–mediated immune suppression in malaria-infected primigravid women

doi: 10.1101/2025.05.21.655391

Figure Lengend Snippet: This figure illustrates the differences in cytokine levels between infected and non-infected women at delivery, highlighting key cytokines involved in the immune response to malaria. (2a) IL-6: Infected women show significantly higher IL-6 levels compared to non-infected women (p-value < 0.001), indicating a heightened pro-inflammatory response. (2b) TNF-α: TNF-α levels are also elevated in infected women (p-value = 0.005), further reflecting an increased inflammatory response. (2c) IFN-γ: There is a significant increase in IFN-γ levels in infected women (p-value = 0.003), suggesting enhanced activation of cellular immunity. (2d) IL-4: Infected women exhibit higher IL-4 levels (p-value < 0.001), indicating a concurrent anti-inflammatory response. (2e) IL-10: The levels of IL-10, a key anti-inflammatory cytokine, are significantly elevated in infected women (p-value < 0.001), which may contribute to immune modulation during malaria infection. (2f) IL-6 / IL-10 Ratio: The IL-6/IL-10 ratio is significantly lower in infected women (p-value = 0.005), indicating a relative dominance of anti-inflammatory over pro-inflammatory responses in these individuals.

Article Snippet: Commercially available cytokine ELISA kits for human samples were used to determine the levels of IL-4 (eBioscience BMS225/2), IL-10 (Invitrogen KHC0101), TNF-α (Invitrogen KHC3011), IL-6 (BioSource Europe KAC1261), and INF-γ (Invitrogen KAC1231).

Techniques: Infection, Activation Assay

Journal: bioRxiv

Article Title: Postpartum cytokine shifts and IL-10–mediated immune suppression in malaria-infected primigravid women

doi: 10.1101/2025.05.21.655391

Figure Lengend Snippet:

Article Snippet: Commercially available cytokine ELISA kits for human samples were used to determine the levels of IL-4 (eBioscience BMS225/2), IL-10 (Invitrogen KHC0101), TNF-α (Invitrogen KHC3011), IL-6 (BioSource Europe KAC1261), and INF-γ (Invitrogen KAC1231).

Techniques:

Journal: bioRxiv

Article Title: Postpartum cytokine shifts and IL-10–mediated immune suppression in malaria-infected primigravid women

doi: 10.1101/2025.05.21.655391

Figure Lengend Snippet: The immune response to Plasmodium falciparum infection involves a delicate balance between pro-inflammatory and anti-inflammatory cytokines. Pro-inflammatory cytokines such as TNF-α and IFN-γ trigger a strong immune response, which is essential for parasite clearance but also increases the risk of severe inflammation and tissue damage. In contrast, IL-10 suppresses excessive inflammation, reducing immune-mediated pathology but facilitating parasite persistence. The clinical outcome depends on this cytokine balance: a dominant pro-inflammatory response can lead to severe malaria (e.g., cerebral malaria, organ damage), whereas a high IL-10 response may promote chronic infection with controlled symptoms.

Article Snippet: Commercially available cytokine ELISA kits for human samples were used to determine the levels of IL-4 (eBioscience BMS225/2), IL-10 (Invitrogen KHC0101), TNF-α (Invitrogen KHC3011), IL-6 (BioSource Europe KAC1261), and INF-γ (Invitrogen KAC1231).

Techniques: Infection

Journal: Advanced Science

Article Title: Increased PRP19 in Hepatocyte Impedes B Cell Function to Promote Hepatocarcinogenesis

doi: 10.1002/advs.202407517

Figure Lengend Snippet: PRP19 suppressed CXCL12 expression in HCC cells. A) The volcano plots of RNA‐sequence in two PRP19 knockdown HCC cells. B) The Venn diagram indicated the co‐differentially expressed genes in two PRP19 knockdown HCC cells. C) The heatmap of key differentially expressed genes in PRP19 knockdown HCC cells. D) B cell migration ability was analyzed by FCM after being treated with CXCL12, C3, CSF1, CCN1, and BCL10. E) CXCL12 expression was analyzed by qPCR in PRP19 knockdown HCC cells. F) CXCL12 protein expression was analyzed by ELISA in PRP19 knockdown HCC cells. G) PRP19 was negatively correlated with CXCL12 mRNA expression in TCGA‐LHC. **p < 0.01, ***p < 0.001 by student's t‐test (D, E, F) and Pearson correlation analysis (G).

Article Snippet: Concentrations of CXCL12 in cell supernatants and mouse serum were analyzed using ELISA kits (eBioscience, USA) according to the manufacturer's instructions.

Techniques: Expressing, Sequencing, Knockdown, Migration, Enzyme-linked Immunosorbent Assay

Journal: Advanced Science

Article Title: Increased PRP19 in Hepatocyte Impedes B Cell Function to Promote Hepatocarcinogenesis

doi: 10.1002/advs.202407517

Figure Lengend Snippet: DDX5 regulates CXCL12 mRNA stability. A) Identifying PRP19 interacted proteins by LC‐MS/MS analysis. B) GO enrichment analysis of identified candidates. C) TOP10 identified candidates who interacted with PRP19. D) DDX5 was highly identified to interact with PRP19. E) Cellular co‐location of PRP19 and DDX5 was explored in HCC cells by IF staining. F) Co‐IP of endogenous PRP19 and DDX5 in HCC cells. G) CXCL12 mRNA level was analyzed by qPCR in DDX5 overexpression and knockdown HCC cells. H) CXCL12 protein level was analyzed by ELISA in DDX5 overexpression and knockdown HCC cells. I) The CXCL12 mRNA stability was explored in DDX5 overexpression and knockdown HCC cells. J) RIP assay was performed to explore the interaction of DDX5 protein and CXCL12 mRNA. K) Cellular co‐location of DDX5 protein and CXCL12 mRNA were explored in HCC cells by IF and FISH staining. *p < 0.05, **p < 0.01, ***p < 0.001 by student's t‐test (G, H, I, J).

Article Snippet: Concentrations of CXCL12 in cell supernatants and mouse serum were analyzed using ELISA kits (eBioscience, USA) according to the manufacturer's instructions.

Techniques: Liquid Chromatography with Mass Spectroscopy, Staining, Co-Immunoprecipitation Assay, Over Expression, Knockdown, Enzyme-linked Immunosorbent Assay