cd3 cd19 antigen pe a ntigen apc  (Miltenyi Biotec)

Journal: MedComm

Article Title: Butyrophilin 3A1 Contributes to Inflammation and Induces a Lupus‐Like Disease by Inhibiting the IL‐38‐Ferroptosis Axis

doi: 10.1002/mco2.70356

Figure Lengend Snippet: BTN3A1 inhibits the IL‐38‐ferroptosis axis and induces CD4 + T cells dysfunction. Naïve CD4 + T cells were isolated from spleens of the BTN3A1 +/+ mice ( N = 5/group), and then were activated. Part of the cells were further stimulated with 100 ng/mL of IL‐38. (A) The mRNA expression of ferroptosis‐related proteins in the cells was detected by qRT‐PCR. (B) Detection of Fe 2+ , glutathione and malondialdehyde levels in above cells reflects cellular ferroptosis. (C, D) The IL‐38‐treated CD4 + BTN3A1 +/+ T cells we intervened with/without Ferrostatin‐1 treatment. Cell proliferation was measured by CCK8 kits and cell apoptosis was measured. Representative flowchart and statistical analysis of apoptosis of different groups of cells are shown. * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001.

Article Snippet: Cell proliferation of CD4 + BTN3A1 +/+ T cells and BTN3A1 +/+ Jurkat T cells was determined by CCK8 kits (Abmole, Houston, USA) in the presence or absence of inhibitors of ferroptosis (Ferrostatin‐1, 2uM) (Monmouth Junction, NJ, USA) for 24 h. Similarly, CD4 + BTN3A1 +/+ T cells and BTN3A1 +/+ Jurkat T cells were treated with/without Ferrostatin‐1 for 24 h, and cell apoptosis was detected using FITC Annexin V Apoptosis Detection Kit I (BD Biosciences, California, USA) and APC Annexin V Apoptosis Detection Kit (Vazyme, Nanjing, China).

Techniques: Isolation, Expressing, Quantitative RT-PCR