Abstract

Dendritic cells (DCs) link the innate and adaptive immune response by capturing antigen to present to and activate naïve T cells. Subsets of DCs vary based on protein expression, which allows for their identification. This research focused on total DCs (CD11c+), and the conventional DC subsets (cDC1 and cDC2). Corticosterone (CORT), a stress-induce glucocorticoid hormone, reduces DC numbers and alters DC function and subsequent T cell responses. The current study quantifies DC recovery after CORT exposure and demonstrates that the loss of DCs can be prevented. Mice were exposed to exogenous CORT in the drinking water for 24 hours. CORT exposure significantly decreased the numbers of all splenic DCs. Mice were then provided varying recovery times (3, 5, or 10 days) post-CORT exposure. DCs quickly returned to normal levels, and even exceeded the percentages in control untreated mice. Studies have shown that injection of mice with anti-CD40 antibody triggers DC maturation and proliferation. Thus, it was hypothesized that injection of anti-CD40 may prevent the CORT-induced loss of DCs. Mice received two injections of anti-CD40 antibody over two days and were then immediately supplied with CORT. When provided anti-CD40 prior to CORT, the loss of DCs was prevented. These studies contribute to the ongoing exploration of the mechanisms underlying the immunological effects of stress-induced glucocorticoids.

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