INTRODUCTION: The low frequency of ectopic germinal center in labial salivary glands of patients with human T-cell leukemia virus type 1 (HTLV-1) antibody-positive Sjögren's syndrome (SS) suggests that HTLV-1 has some effects on follicular dendritic cells (FDCs). METHODS: We used flow cytometry, immunofluorescence, and enzyme-linked immunosorbent assays (ELISAs) to investigate the direct effect of HTLV-1 on B-cell activating factors produced by established FDC like cells obtained from excised human tonsils. We then measured the serum B-cell activating factor (BAFF) and C-X-C motif ligand (CXCL) 13 concentrations of the HTLV-1-seropositive SS patients and the HTLV-1-seronegative SS patients by ELISA. RESULTS: Among the 31 isolated specimens, 22 showed morphological characteristics of FDCs. Day 2-cultured specimens showed expressions of CD14, CD23, CD40, intracellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1. After 2 weeks, 12 of these specimens expressed ICAM-1, FDC, and fibroblast cell marker. Intracellular BAFF and CXCL13 were constitutively expressed regardless of stimulation. After direct coculture with the HTLV-1-infected T-cell line HCT-5 or MT-2, the BAFF and CXCL13 expressions on the FDC-like cells were decreased in accord with the increased number of HCT-5 and MT-2 cells with styliform change and without HTLV-1 Gag protein expression. Interferons upregulated the concentration of BAFF (but not CXCL13) in the culture supernatant, which showed a declining trend under the presence of HCT-5 or MT-2. The serum concentrations of BAFF and CXCL13 in the HTLV-1-seropositive SS patients were lower than those of the HTLV-1 seronegative SS patients. CONCLUSIONS: HTLV-1 partially inhibited the BAFF and CXCL13 expressions of established FDC-like cells.
INTRODUCTION: The low frequency of ectopic germinal center in labial salivary glands of patients with human T-cell leukemia virus type 1 (HTLV-1) antibody-positive Sjögren's syndrome (SS) suggests that HTLV-1 has some effects on follicular dendritic cells (FDCs). METHODS: We used flow cytometry, immunofluorescence, and enzyme-linked immunosorbent assays (ELISAs) to investigate the direct effect of HTLV-1 on B-cell activating factors produced by established FDC like cells obtained from excised human tonsils. We then measured the serum B-cell activating factor (BAFF) and C-X-C motif ligand (CXCL) 13 concentrations of the HTLV-1-seropositive SSpatients and the HTLV-1-seronegative SS patients by ELISA. RESULTS: Among the 31 isolated specimens, 22 showed morphological characteristics of FDCs. Day 2-cultured specimens showed expressions of CD14, CD23, CD40, intracellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1. After 2 weeks, 12 of these specimens expressed ICAM-1, FDC, and fibroblast cell marker. Intracellular BAFF and CXCL13 were constitutively expressed regardless of stimulation. After direct coculture with the HTLV-1-infected T-cell line HCT-5 or MT-2, the BAFF and CXCL13 expressions on the FDC-like cells were decreased in accord with the increased number of HCT-5 and MT-2 cells with styliform change and without HTLV-1Gag protein expression. Interferons upregulated the concentration of BAFF (but not CXCL13) in the culture supernatant, which showed a declining trend under the presence of HCT-5 or MT-2. The serum concentrations of BAFF and CXCL13 in the HTLV-1-seropositive SSpatients were lower than those of the HTLV-1 seronegative SS patients. CONCLUSIONS:HTLV-1 partially inhibited the BAFF and CXCL13 expressions of established FDC-like cells.