Abstract: TH-PO894
Age-Dependent Production of Highly Apoptosis-Resistant CD31 – Memory-Tresps May Cause Chronic Inflammatory Conditions in Dialysis Patients
Session Information
- Dialysis: Infection
November 02, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Dialysis
- 610 Dialysis: Infection
Authors
- Schaier, Matthias, University of Heidelberg, Heidelberg, Germany
- Leick, Angèle, University of Heidelberg, Heidelberg, Germany
- Kälble, Florian, University of Heidelberg, Heidelberg, Germany
- Morath, Christian, University of Heidelberg, Heidelberg, Germany
- Sommerer, Claudia, University of Heidelberg, Heidelberg, Germany
- Zeier, Martin G., University of Heidelberg, Heidelberg, Germany
- Steinborn-Kroehl, Andrea, University of Heidelberg, Heidelberg, Germany
Background
Dialysis patients have an increased susceptibility for chronic inflammation. In addition, an increased risk for virus-associated cancers and atherosclerotic diseases are documented.
Methods
We analyzed whether age-related differences in the differentiation of both recent-thymic-emigrant-(RTE)- regulatory (Tregs) and RTE-responder T cells (Tresps) into CD31--memory Tregs/Tresps led to differences in the suppressive activity of naïve and memory Tregs on autologous Tresps between healthy volunteers (n= 89) and dialysis patients (n=80).
Results
Our findings suggest, that the thymic release of RTE-Tregs decreases with age and thereby causes their enhanced differentiation via CD31+-memory Tregs into CD31--memory Tregs, so that the suppressive activity of both naïve and memory-Tregs is maintained with age in healthy controls. In addition, the decreasing thymic release of RTE-Tresps may cause their enhanced differentiation via MN-Tresps into CD31--memory-Tresps. Thus, the reactivity of the total Tresp pool may be weakened with age, as the resulting CD31--memory- Tresps may be much more sensitive to apoptosis. Presumably, both effects contribute to the fact that the functional activity of Tregs increases with age in healthy volunteers. Dialysis patients exhibit an increased RTE-Treg differentiation via CD31+-memory Tregs which may enhance the suppressive activity of both naïve CD45RA+- and CD45RA--memory-Tregs, especially in young individuals. However, the differentiation of RTE-Tresps via MN-Tresps, seen in healthy volunteers, could not be detected in dialysis patients. Instead, there was an age-dependent increase in the differentiation via CD31+-memory Tresps into CD31--memory Tresps in dialysis patients. This effect may strengthen the functionality of Tresps with age and explain why Tregs of elderly dialysis patients show difficulties suppressing autologous Tresps, but preserve the ability to suppress non-autologous Tresps of healthy volunteers.
Conclusion
The aging immune system sustainably suppresses autoimmunity, but favors the incidence of inflammation. In contrast, the increased age-dependent production of highly apoptosis-resistant CD31--memory-Tresps in dialysis patients may cause chronic inflammatory conditions in these patients.