T lymphocytes promote autoimmune‐associated hypertension

Abstract

Evidence suggests that essential hypertension has autoimmune origins. We tested whether T cells, important mediators of autoimmunity, contribute to the prevalent hypertension in the autoimmune inflammatory disorder systemic lupus erythematosus (SLE). Female mice with active SLE (NZBWF1 with albuminuria ≥ 100 mg/dL) or control mice (NZW) were treated with the T cell receptor antibody (anti‐CD3) or anti‐IgG for 3–4 weeks (intranasally; 25 μg/week). Renal cortical expression of CD3 antigen was increased in SLE mice (p=0.03) and splenic CD3+CD4+ T cells were increased in SLE mice compared to controls (19 ± 2% vs. 14 ± 1% gated, p=0.04). Spleen weight was increased in SLE mice compared to controls, and was normalized by anti‐CD3. Blood pressure (mmHg) was increased in SLE mice compared to controls (155 ± 3 vs. 112 ± 4, p=0.001), and was lower in SLE mice (137 ± 6; p=0.01) but not controls (117±2) after anti‐CD3. Albuminuria (mg/mg creatinine) was increased in SLE mice compared to controls (500 ± 290 vs. 0.05 ± 0.01; p=0.01), and was reduced in SLE mice (50 ± 37; p=0.03) but not controls (0.06 ± 0.01) after anti‐CD3. Renal cortical IL‐17 receptor expression was increased in SLE mice compared to controls, and was reduced after anti‐CD3. These data suggest that T cell‐mediated inflammation contributes to hypertension and renal injury during SLE. Support: AHA4350019 (KWM), HL085907, HL092284, HL085907S1 (MJR), HL051971 (UMMC‐Phys)