B lymphocyte subsets in patients with rhinoscleroma.

OBJECTIVE: To identify the presence of B lymphocytes in the rhinoscleroma granulomas as a possible precursor of plasma cells, whose presence has always been described but whose role is still unclear. STUDY DESIGN: Case series with chart review. SETTING: Sapienza University of Rome. METHODS: The study was carried out on 6 patients (3 women, 3 men). The following parameters were examined for each patient: clinical manifestations, number of leukocytes, lymphocytes and lymphocyte subsets (CD3+, CD4+, CD8+, and CD19+) in blood samples, time from the onset of symptoms, biopsies, and expression of CD3, CD4, CD8, and CD20 antigens in tissue samples with immunohistochemical techniques. RESULTS: In this study, the values of CD3+, CD4+, and CD8+ T lymphocyte subsets in venous peripheral blood are in line with previously reported data, whereas CD19+ lymphocyte cells tended to show an ambiguous behavioral pattern. In tissue samples, approximately one-third of the T lymphocyte population showed a CD3+/CD8+ immunophenotype (cytotoxic/suppressor), and two-thirds of the T lymphocytes expressed a CD3+/CD4+ immunophenotype (helper/inducer). The authors also identified an unexpected large amount of CD20+ non-plasmacellular B cells in addition to the plasma cells usually detected in rhinoscleroma biopsies. CONCLUSIONS: This study demonstrates the presence of B lymphocytes in rhinoscleroma tissue. It is presumable that the mature B cells activated by antigenic stimulation of Klebsiella rhinoscleromatis are the precursors of the plasma cells typically found in the granuloma of rhinoscleroma.

Alterations in the T-lymphocyte subpopulation in patients with rhinoscleroma.

T-lymphocyte subpopulations were studied in a group of patients with rhinoscleroma due to Klebsiella rhinoscleromatis. The data demonstrated that these patients had a significantly greater number of T-suppressor/cytotoxic lymphocytes than did clinically healthy individuals. This finding correlated with a diminished response to the T-cell mitogen concanavalin A. The evidence indicated that the T-cell response of these patients was decreased and may reflect the host's response to the bacterial invader, thus explaining the chronicity of the disease.