An immunohistological analysis of 13 idiopathic subglottic stenosis (iSGS) excisions: a single centre study.

Idiopathic subglottic stenosis (iSGS) is a rare disease that primarily affects young and middle-aged females. There is a lack of data investigating the pathological mechanisms of this disease. This study aimed to provide histological and immunohistochemical evidence of the differences between specimens from iSGS patients and healthy individuals. Using histological staining, tracheal mucosa specimens from patients with iSGS and healthy individuals were assessed based on abnormal changes, such as fibrosis, acute inflammation, chronic inflammation, perivascular inflammation, and glandular inclusions. Immunohistochemical analyses were performed using Giemsa, CD20 antibody B cell, CD5, CD4, CD8, CD56, CD68, CD25, TIA-1 and Granzyme B staining. For the control group, tracheal biopsies were obtained during bronchoscopic procedures conducted for diagnostic or therapeutic purposes unrelated to iSGS. These individuals did not have tracheal stenosis and were considered healthy in terms of their tracheal condition. Informed consent for the collection of samples for research purposes was obtained from all control group participants prior to the procedure. Thirteen patients with iSGS and five healthy participants were included. A comparison of immune cell populations between the iSGS and control groups revealed significant differences. Lymphocytes were numerously present in 77% of the cases in the iSGS group and few in 60% of the cases in the control group (p = 0.006). In 12 out of 13 (92.31%) cases, we observed inflammatory infiltrates, mainly CD4 T cells and a few cytotoxic CD8 T cells. B cells were present in 11 out of 13 (84.62%) cases but were mostly found in smaller numbers than T cells. Follicle formation was observed in only 2 out of 13 (15.38%) samples. We were not able to detect obvious immunohistochemical features in our patients with iSGS. However, some standard features were present within the samples showing a clear inflammatory state. Patients with iSGS showed a notably higher proportion of lymphocytes compared to control participants. The increase in lymphocytes was largely driven by T cells, with CD4-positive T-helper cells being more numerous than cytotoxic T cells. The clinical history of the patient collective was heterogeneous and did not allow for any conclusions to be drawn regarding the aetiology. Further studies are needed to characterize the tissues to clearly define the aetiology of iSGS.