Eosinophils infiltrate thyroids, but have no apparent role in induction or resolution of experimental autoimmune thyroiditis in interferon‐γ − /− mice

Summary Granulomatous experimental autoimmune thyroiditis (G‐EAT) is induced by mouse thyroglobulin (MTg)‐sensitized splenocytes activated with MTg and interleukin (IL)‐12. Our previous studies showed that, when used as donors and recipients, interferon (IFN)‐γ −/− and wild‐type (WT) DBA/1 mice both develop severe G‐EAT. Thyroid lesions in IFN‐γ −/− mice have many eosinophils and few neutrophils, while those in WT mice have extensive neutrophil infiltration and few eosinophils. Thyroid lesions in IFN‐γ −/− mice consistently resolve by day 40–50, whereas those in WT mice have ongoing inflammation and fibrosis persisting for more than 60 days. To determine if the extensive infiltration of eosinophils in thyroids of IFN‐γ −/− mice contributes to thyroid damage and/or early resolution of G‐EAT, anti‐IL‐5 was used to inhibit migration of eosinophils to thyroids. G‐EAT severity was compared at day 20 and day 40–50 in IFN‐γ −/− recipients given anti‐IL‐5 or control immunoglobulin G (IgG). Thyroids of anti‐IL‐5‐treated IFN‐γ −/− mice had few eosinophils and more neutrophils at day 20, but G‐EAT severity scores were comparable to those of control IgG‐treated mice at both day 20 and day 40–50. Expression of chemokine (C‐X‐C motif) ligand 1 (CXCL1) mRNA was higher and that of chemokine (C‐C motif) ligand 11 (CCL11) mRNA was lower in thyroids of anti‐IL‐5‐treated IFN‐γ −/− mice. IL‐5 neutralization did not influence mRNA expression of most cytokines in IFN‐γ −/− mice. Thus, inhibiting eosinophil migration to thyroids did not affect G‐EAT severity or resolution in IFN‐γ −/− mice, suggesting that eosinophil infiltration of thyroids occurs as a consequence of IFN‐γ deficiency, but these cells have no apparent pathogenic role in G‐EAT.