| Autor: |
Nikolajczyk BS; Department of Pharmacology and Nutritional Sciences and Barnstable Brown Diabetes Center, University of Kentucky, Lexington, KY, USA. barb.nik@uky.edu., Dawson DR 3rd; Department of Oral Health Practice, Division of Periodontology, College of Dentistry, University of Kentucky, Lexington, KY, USA. |
| Jazyk: |
angličtina |
| Zdroj: |
Advances in experimental medicine and biology [Adv Exp Med Biol] 2019; Vol. 1197, pp. 45-54. |
| DOI: |
10.1007/978-3-030-28524-1_4 |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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