T Cell-Derived IL-17A Induces Vascular Dysfunction via Perivascular Fibrosis Formation and Dysregulation of ^⋅NO/cGMP Signaling

Figure 2

T cell-specific IL-17A overexpression does not result in an infiltration of inflammatory cells into the aortic wall; nevertheless, CD11b⁺ cells are more reactive. (a) Flow cytometric analysis of aortas from CD4-IL-17A^ind/+ compared to IL-17A^ind/+ control mice. Dot plot shows gating strategy of aortic samples. Cells were pregated on living cells and gated on CD45.2⁺, CD90.2^-, CD11b⁺, F4/80⁺, and either Ly6G⁺Ly6C⁺ neutrophils or Ly6C^single+ monocytes. Quantitative analysis of aortic flow cytometric analysis; mice per group; either Student’s unpaired -test or Mann–Whitney -test. (b) ROS/RNS measurement in whole peripheral blood was performed after stimulation with PDBu for 20 minutes; repeated measurements of pooled samples; mice per group; unpaired Student’s -test. (c) ROS/RNS detection in isolated CD11b⁺ splenocytes after 20 min stimulation with PDBu; ; Student’s unpaired -test. Data are presented as .

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