108. Decreased regulatory T cell populations in an in vitro stress model using normal human PBMC
Autor: | Kristina E. Rehm, Gailen D. Marshall, D.D. Montgomery |
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Rok vydání: | 2012 |
Předmět: |
medicine.medical_specialty
medicine.diagnostic_test Endocrine and Autonomic Systems Regulatory T cell T cell Immunology Cell Biology Peripheral blood mononuclear cell In vitro Flow cytometry Behavioral Neuroscience Immune system medicine.anatomical_structure Endocrinology Internal medicine medicine Dexamethasone medicine.drug |
Zdroj: | Brain, Behavior, and Immunity. 26:S30 |
ISSN: | 0889-1591 |
DOI: | 10.1016/j.bbi.2012.07.132 |
Popis: | The regulatory arm of the immune system is composed of several types of cells, including CD4 + CD25hiFoxP3 + Treg cells, Tr1 (CD4 + IL-10-producing) cells, and Th3 (CD4 + TGFbeta-producing) cells. These cells collectively regulate the responses of effector T cells, including Th1 and Th2. We have previously shown that both short-term (24 h) and long-term (11 day) exposure of lymphocytes to physiological stress-equivalent concentrations (10–8 M) of dexamethasone (DEX; a laboratory analog of cortisol) results in a significant decrease of the Th1/Th2 ratio, but it is unknown how stress affects the regulatory cells of the immune system. PBMC from healthy donors ( n = 18) were incubated with tetanus toxoid, IL-2, and with or without DEX. The phenotype of the various T cell populations was assessed by multicolor flow cytometry after 24 h, 5 days, and 11 days. Consistent with previous data, Th1/Th2 ratio was significantly decreased by DEX at each time point tested. Treg, Tr1, and Th3 cell populations were all significantly decreased by DEX after 24 h exposure. On days 5 and 11, there were no significant effects of DEX incubation on Tr1 and Th3 cells, but there was a significant increase in the number of Treg cells. These data suggest that the stress hormone-induced short term suppression of regulatory T cell subpopulations may be a mechanism for the altered Th1/Th2 balance seen in long term cultures. |
Databáze: | OpenAIRE |
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