Abstract
New strategies are critically needed to counter uncontrolled periodontal infection and inflammation in obesity-associated type 2 diabetes (T2D). However, mechanisms that explain the relationship between periodontitis (PD) and T2D remain poorly understood. Several lines of evidence indicate that destructive immune responses potentiate periodontitis (PD) in T2D. B cells are abundant in periodontal lesions, and our data show that B cells are required for PD in obese/insulin resistant but not lean/normoglycemic mice. In mice and in people, T2D-primed B cells supported Th17 cytokine profiles, but B cells had a modest effect on T-cell function in samples from normoglycemic individuals. Given the recently appreciated importance of Th17 cells in PD outside a T2D milieu, our data raise the possibility that B cells indirectly promote T2D-potentiated PD through support of Th17 cells, which in turn directly promote PD. Data herein thereby suggest unexpected mechanisms that explain the clinical observation that T2D potentiates PD.
Original language | English |
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Title of host publication | Advances in Experimental Medicine and Biology |
Pages | 45-54 |
Number of pages | 10 |
DOIs | |
State | Published - 2019 |
Publication series
Name | Advances in Experimental Medicine and Biology |
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Volume | 1197 |
ISSN (Print) | 0065-2598 |
ISSN (Electronic) | 2214-8019 |
Bibliographical note
Publisher Copyright:© 2019, Springer Nature Switzerland AG.
Keywords
- B cells
- Inflammation
- Metabolic disease
- Obesity
- Periodontitis
- Th17 cells
ASJC Scopus subject areas
- General Biochemistry, Genetics and Molecular Biology