ArticleMolecular medicine reports2017
Frequency and distribution of CD4+CXCR5+ follicular B helper T cells within involved tissues in IgG4‑related ophthalmic disease.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Single-cell multi-omics analysis revealed the expansion of age-associated B cells in the pancreas of type 1 autoimmune pancreatitis patients.Genome medicine · 2025Article
- T Cell Roles and Activity in Chronic Sclerosing Sialadenitis as IgG4-Related Disease: Current Concepts in Immunopathogenesis.Autoimmune diseases · 2022Review
- Tertiary lymphoid structures in the primary tumor site of patients with cancer-associated myositis: A case-control study.Frontiers in medicine · 2022Article
- IgG4-Related Disease: Beyond Glucocorticoids.Drugs & aging · 2018Review
- T Follicular Helper Cells in Autoimmune Disorders.Frontiers in immunology · 2018Review
- Increased frequency of circulating Tfh cells in patients with acute pancreatitis.International journal of clinical and experimental pathology · 2018Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immonoglobulin G4‑related ophthalmic disease (IgG4‑ROD) is a IgG4‑RD and exhibits two main characteristics: Fibrosis that is not necessarily marked histopathologically; and frequent formation of germinal centers (GCs). Follicular B helper T (Tfh) cells are now recognized as the true helper cells for B cells in antibody responses. In the present study, the profile and distribution of Tfh cells in involved tissues from patients with IgG4‑ROD was compared to those of type 1 autoimmune pancreatitis (AIP) and patients with IgG4‑related lymphadenopathy (IgG4‑RL). A total of 7 patients with IgG4‑ROD, 7 patients with type 1 AIP or IgG4‑RL and 7 IgG4‑negative controls were evaluated. The expression of Tfh‑cell immunological proteins, the inducible T‑cell costimulator, B‑cell lymphoma 6 protein, C‑X‑C chemokine receptor type 5 (CXCR5) and interleukin‑21 (IL‑21) in affected tissues was analyzed using immunohistochemical staining and dual immunofluorescence. It was demonstrated that patients with IgG4‑RD exhibited a significantly increased number of CD4+CXCR5+ Tfh cells compared with the IgG4‑negative controls. Furthermore, CD4+CXCR5+ Tfh cells were detected in and outside of GCs in patients with IgG4‑ROD and IgG4‑RLF, whereas CD4+CXCR5+ Tfh cells were randomly distributed in areas demonstrating type 1 AIP. Fewer CD4+CXCR5+ Tfh cells were observed in patients with type 1 AIP compared with patients with IgG4‑ROD and IgG4‑RL. In addition, increased expression of IL‑21 was observed in patients with IgG4‑ROD and IgG4‑RL compared with type 1 AIP. IL‑21 expression was positively correlated with the IgG4/IgG ratio in immunohistochemically‑positive cells. The results of the present study indicate that Tfh cells are involved in the histopathological pathogenesis of IgG4‑RD and may serve a different role in IgG4‑ROD and type 1 AIP. Tfh cells may serve a direct role in the IL‑21‑mediated pathogenesis of IgG4‑ROD.
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