Objectives: Evidence suggests eosinophils may be acting as antigen-presenting cells (APCs) by presenting antigen to T cells. We investigated the surface proteins of eosinophils and T cells in the esophageal biopsies of patients with eosinophilic esophagitis (EoE), patients with gastroesophageal reflux disease (GERD), and healthy controls (HCs).
Methods: Subjects were categorized as EoE, GERD, or HC. In esophageal tissue, EG2+ eosinophils were stained for the APC markers, CD40 or CD80, via immunohistochemistry. CD3+ T cells were stained for costimulatory markers, CD40L or CD28, and for activation markers, CD69 or CD134, via immunofluorescence or immunohistochemistry.
Results: Eosinophils stained with CD40 and CD80. The number of EG2+CD40+ cells was increased in EoE (mean 19.1 ± 14.8 cells/high-power field [HPF], n = 11), compared with GERD (mean 0.13 ± 0.19 cells/HPF, n = 5, P < 0.01) and HC (mean 0.3 ± 0.7 cells/HPF, n = 5, P < 0.01). There was an elevation in EG2+CD80+ cells in EoE (mean 18.1 ± 16.2 cells/HPF, n = 10), GERD (mean 1.7 ± 2.8 cells/HPF, n = 6, P < 0.01), or HC (mean 0.8 ± 1.3 cells/HPF, n = 6, P < 0.01). CD3+ T cells stained with CD40L (not quantified). CD3+ T cells stained with CD28 at elevated levels in EoE (mean 14 ± 8.7 cells/HPF, n = 9) versus GERD (mean 3.3 ± 1.2 cells/HPF, n = 6, P < 0.05) or HC (mean 3.0 ± 3.2 cells/HPF, n = 7, P < 0.01). The number of CD3+CD69+ cells was highest in EoE (mean 14.8 ± 7.5 cells/HPF, n = 6) versus GERD (mean 0.8 ± 0.9 cells/HPF, n = 6, P < 0.001) or HC (mean 2.7 ± 2.5 cells/HPF, n = 6, P < 0.001).
Conclusions: We show that esophageal eosinophils express CD40 and CD80, and T cells with CD40L, CD28, and CD69. The number of double-stained cells was higher in EoE in comparison to control groups. These data support the hypothesis that eosinophils in EoE may act as APCs, activating T cells.
*Department of Pediatrics, Division of Gastroenterology, Hepatology and Nutrition
†Department of Pediatrics, Division of Allergy and Immunology, Stanford University Medical Center, Lucile Packard Children's Hospital, Palo Alto
‡Pediatric Center for Inflammatory Bowel Disorders, California Pacific Medical Center, San Francisco, California.
Address correspondence and reprint requests to Minou Le-Carlson, MD, Stanford University School of Medicine, 750 Welch Rd, Suite 116, Palo Alto, CA 94304 (e-mail: email@example.com).
Received 8 June, 2012
Accepted 21 September, 2012
This study was supported by the Transplant and Tissue Engineering Center for Excellence Endowment Fund (Le-Carlson, Seki) and the Harry Lyon Machen Fellowship Award (Le-Carlson).
The authors report no conflicts of interest.