C A Rubio1, T Ichiya2, P T Schmidt2. 1. Department of Pathology, Karolinska Institute and University Hospital, Stockholm, Sweden. 2. Department of Medicine, Center for Digestive Diseases, Karolinska Institute and University Hospital, Stockholm, Sweden.
Abstract
AIMS: To report four histological-immunohistochemical oesophagitis phenotypes. METHODS: Oesophageal biopsies from 311 patients were stained with H&E and with CD3, a T cell marker. Additional immunohistochemical stains (n=413) were performed in 77 cases. RESULTS: Four histological-immunohistochemical oesophagitis phenotypes were recorded: lymphocytic oesophagitis (LyE, ≥40 CD3+ lymphocytes/HPF in CD3 immunostain), eosinophilic oesophagitis (EoE, ≥15 eosinophils/HPF in H&E stain), lymphocytic infiltration (≤39 CD3+/HPF) and compound lymphocytic oesophagitis-eosinophilic oesophagitis (Co LyE-EoE). At index biopsy, 28.3% (n=88) had LyE, 21.2% (n=66) EoE, 10.6% (n=33) Co LyE-EoE and 39.9% (n=124) lymphocytic infiltration. A persistent oesophagitis phenotype was found in 42.5% (37/87) in the first follow-up biopsy, in 34.4% (21/61) in the second follow-up biopsy and in 48.1% (26/54) in the third follow-up biopsy. Using βF1 immunostain, two different surface T cell receptors were detected in LyE and Co Lye-EoE: one having ≥40 βF1+/HPF (βF1+ high) and the other having <39 βF1+/HPF (βF1+ low). CONCLUSIONS: Based on the literature regarding the significance of intraepithelial lymphocytes (IELs) in the initiation of EoE, we submit that the IEL phenotypes in LyE might differ from those found in EoE as they were unable to elicit the same eosinophilic response. Recent studies disclosed that group 2 innate lymphocytes (ILC2s), enriched in EoE, remain undetected in CD3 immunostain as they lack surface markers for T, B, natural killer (NK) or NK T cells. If ILC2s also participate in the lymphocytic infiltration of EoE, then the frequency of cases with Co LyE-EoE here reported might have been much higher. The four oesophagitis phenotypes described are easy to recognise, provided that the dual staining procedure (H&E-CD3) is implemented. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.
AIMS: To report four histological-immunohistochemical oesophagitis phenotypes. METHODS: Oesophageal biopsies from 311 patients were stained with H&E and with CD3, a T cell marker. Additional immunohistochemical stains (n=413) were performed in 77 cases. RESULTS: Four histological-immunohistochemical oesophagitis phenotypes were recorded: lymphocytic oesophagitis (LyE, ≥40 CD3+ lymphocytes/HPF in CD3 immunostain), eosinophilic oesophagitis (EoE, ≥15 eosinophils/HPF in H&E stain), lymphocytic infiltration (≤39 CD3+/HPF) and compound lymphocytic oesophagitis-eosinophilic oesophagitis (Co LyE-EoE). At index biopsy, 28.3% (n=88) had LyE, 21.2% (n=66) EoE, 10.6% (n=33) Co LyE-EoE and 39.9% (n=124) lymphocytic infiltration. A persistent oesophagitis phenotype was found in 42.5% (37/87) in the first follow-up biopsy, in 34.4% (21/61) in the second follow-up biopsy and in 48.1% (26/54) in the third follow-up biopsy. Using βF1 immunostain, two different surface T cell receptors were detected in LyE and Co Lye-EoE: one having ≥40 βF1+/HPF (βF1+ high) and the other having <39 βF1+/HPF (βF1+ low). CONCLUSIONS: Based on the literature regarding the significance of intraepithelial lymphocytes (IELs) in the initiation of EoE, we submit that the IEL phenotypes in LyE might differ from those found in EoE as they were unable to elicit the same eosinophilic response. Recent studies disclosed that group 2 innate lymphocytes (ILC2s), enriched in EoE, remain undetected in CD3 immunostain as they lack surface markers for T, B, natural killer (NK) or NK T cells. If ILC2s also participate in the lymphocytic infiltration of EoE, then the frequency of cases with Co LyE-EoE here reported might have been much higher. The four oesophagitis phenotypes described are easy to recognise, provided that the dual staining procedure (H&E-CD3) is implemented. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.