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T cell Polarization toward TH2/TFH2 and TH17/TFH17 in Patients with IgG4-related Disease.
- Source :
- Frontiers in Immunology; 3/13/2017, Vol. 8, p1-10, 10p
- Publication Year :
- 2017
-
Abstract
- IgG4-related disease (IgG4-RD) is a fibro-inflammatory disorder involving virtually every organ with a risk of organ dysfunction. Despite recent studies regarding B cell and T cell compartments, the disease’s pathophysiology remains poorly understood. We examined and characterized subsets of circulating lymphocytes in untreated patients with active IgG4-RD. Twenty-eight consecutive patients with biopsy-proven IgG4-RD were included in a prospective, multicentric study. Lymphocytes’ subsets were analyzed by flow cytometry, with analysis of T<subscript>H</subscript>1/T<subscript>H</subscript>2/T<subscript>H</subscript>17, T<subscript>FH</subscript> cells, and cytokine release by peripheral blood mononuclear cells. Results were compared to healthy controls and to patients with primary Sjögren's syndrome. Patients with IgG4-RD showed an increase of circulating T regulatory, T<subscript>H</subscript>2, T<subscript>H</subscript>17, and CD4+CXCR5+PD1+ T<subscript>FH</subscript> cell subsets. Accordingly, increased levels of IL-10 and IL-4 were measured in IgG-RD patients. T<subscript>FH</subscript> increase was characterized by the specific expansion of T<subscript>FH</subscript>2 (CCR6-CXCR3-), and to a lesser extent of T 17 (CCR6+ - FH CXCR3 ) cells. Interestingly, CD4+CXCR5+PD1+ T<subscript>FH</subscript> cells normalized under treatment. IgG4-RD is characterized by a shift of circulating T cells toward a T<subscript>H</subscript>2/T<subscript>FH</subscript>2 and T<subscript>H</subscript>17/T<subscript>FH</subscript>17 polarization. This immunological imbalance might be implicated in the disease’s pathophysiology. Treatment regimens targeting such T cells warrant further evaluation. [ABSTRACT FROM AUTHOR]
- Subjects :
- T helper cells
IMMUNOGLOBULIN G
PATHOLOGICAL physiology
DISEASES
Subjects
Details
- Language :
- English
- ISSN :
- 16643224
- Volume :
- 8
- Database :
- Complementary Index
- Journal :
- Frontiers in Immunology
- Publication Type :
- Academic Journal
- Accession number :
- 121780455
- Full Text :
- https://doi.org/10.3389/fimmu.2017.00235