Kyoung-Hee Sohn1,2, Jongho Ham3,4, Soo Jie Chung1,2, Hye-Ryun Kang1,2, Hye Young Kim5,6,7. 1. Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea. 2. Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul National University College of Medicine, Seoul, Republic of Korea. 3. Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Republic of Korea. 4. Laboratory of Mucosal Immunology in Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Republic of Korea. 5. Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul National University College of Medicine, Seoul, Republic of Korea, hykim11@snu.ac.kr. 6. Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Republic of Korea, hykim11@snu.ac.kr. 7. Laboratory of Mucosal Immunology in Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Republic of Korea, hykim11@snu.ac.kr.
Abstract
BACKGROUND: Immunoglobulin G4-related disease (IgG4-RD) is a systemic immunological disorder characterized by fibro-inflammatory conditions; however, the pathobiology of IgG4-RD has not been fully identified. OBJECTIVE: This study aimed to analyze systemic differences of innate and adaptive immune cells from healthy controls and patients with IgG4-RD. METHODS: Healthy controls (n = 9) and IgG4-RD patients (n = 7) were recruited with informed consent. Peripheral blood was collected from healthy controls and IgG4-RD patients, and three blood samples from IgG4-RD patients were re-collected two months after the last rituximab (RTX) treatment. The various immune cells and cytokine productions were measured by flow cytometry. RESULTS: Blood CD14+ monocytes and steady-state follicular helper T cells were increased in patients with IgG4-RD. However, there were no changes in other immune cell populations, including B cells, CD4 T cells, CD8 T cells, and innate lymphoid cells. Also, the TGF-β-producing CD14+ monocytes were significantly augmented in patients with IgG4-RD. Two months after RTX treatment, total B cells (CD19+) were depleted; however, the expressions of TGF-β from CD14+ monocytes remained unchanged. CONCLUSION: These findings showed that IgG4-RD is related to the increment of CD14+ monocytes. Besides, controlling increased TGF-β-producing CD14+ monocytes with RTX treatment might be a conducive way to regulate IgG4-RD.
BACKGROUND: Immunoglobulin G4-related disease (IgG4-RD) is a systemic immunological disorder characterized by fibro-inflammatory conditions; however, the pathobiology of IgG4-RD has not been fully identified. OBJECTIVE: This study aimed to analyze systemic differences of innate and adaptive immune cells from healthy controls and patients with IgG4-RD. METHODS: Healthy controls (n = 9) and IgG4-RD patients (n = 7) were recruited with informed consent. Peripheral blood was collected from healthy controls and IgG4-RD patients, and three blood samples from IgG4-RD patients were re-collected two months after the last rituximab (RTX) treatment. The various immune cells and cytokine productions were measured by flow cytometry. RESULTS: Blood CD14+ monocytes and steady-state follicular helper T cells were increased in patients with IgG4-RD. However, there were no changes in other immune cell populations, including B cells, CD4 T cells, CD8 T cells, and innate lymphoid cells. Also, the TGF-β-producing CD14+ monocytes were significantly augmented in patients with IgG4-RD. Two months after RTX treatment, total B cells (CD19+) were depleted; however, the expressions of TGF-β from CD14+ monocytes remained unchanged. CONCLUSION: These findings showed that IgG4-RD is related to the increment of CD14+ monocytes. Besides, controlling increased TGF-β-producing CD14+ monocytes with RTX treatment might be a conducive way to regulate IgG4-RD.
Authors: M Yamamoto; S Harada; M Ohara; C Suzuki; Y Naishiro; H Yamamoto; H Takahashi; K Imai Journal: Rheumatology (Oxford) Date: 2004-10-27 Impact factor: 7.580