Numerous mechanisms have been suggested for the development of subglottic stenosis. This study sought serum antibody and cricoid cartilage immunohistologic evidence of an autoimmune process. The autoimmune hypothesis is that subglottic inflammation may extend into the cricoid cartilage, degrade the extracellular matrix and expose normally-sequestered type II collagen to the afferent arm of the immune system. The resultant anti-collagen antibodies are hypothesized to contribute to further injury and scarring. Specimens were obtained from 10 patients. Immunofluorescent stains for antibodies in histologic specimens, and serum antibodies to type II and type IX collagen were sought. No evidence for an autoimmune process was found in these specimens with the techniques used. The negative findings may be attributable to the autoimmune process being inactive at the mature stage of the disease in the patients studied.