The Role of Adenosine A2A Receptor on the Induction of Regulatory T Cells in Uveitis

Presenter

June Ahn

Campus

UMass Amherst

Sponsor

Elizabeth Mearls, Department of Biochemistry and Molecular Biology, UMass Amherst

Schedule

Session 4, 2:30 PM - 3:15 PM [Schedule by Time][Poster Grid for Time/Location]

Location

Poster Board A77, Campus Center Auditorium, Row 4 (A61-A80) [Poster Location Map]

Abstract

Autoimmune uveitis is a complex ocular condition wherein the immune system attacks the vascular region of the eye, posing a significant threat to vision. The ability of regulatory T cells (Tregs) to suppress immune responses in inflammatory diseases like uveitis underscores the importance of their induction. It is believed that Tregs are formed through the melanocortin-adenosinergic-dependent counter-conversion of effector T cells in interaction with antigen-presenting cells (APCs). However, the eye's unique immunity privilege, which curbs inflammatory responses, complicates this counter-conversion process. Previous studies have linked the upregulation of B-cell lymphoma 2 (BCL-2), an anti-apoptotic protein, which can be achieved through stimulation of the A2Ar receptor, to enhanced Treg function. This study hypothesizes that the A2Ar receptor upregulates BCL-2 in inflammatory T cells. This upregulation facilitates the conversion of effector T cells into Tregs, circumventing ocular immunity. Spleens from uveitis-immunized A2Ar knockout and wild-type mice were treated with A2Ar agonists and subsequently examined for BCL-2 and T cell markers using flow cytometry. Significant differences in BCL-2 expression were observed only in non-T cell (CD4-) events, with wild-type mice exhibiting higher levels of BCL-2. Further, BCL-2 expression increased upon stimulation of the A2Ar receptor with CGS, an A2Ar agonist. These results suggest that A2Ar primarily affects BCL-2 expression in CD4- cells, indicating that dendritic cells, not effector T cells, may be given a survival signal through BCL-2 to aide in the conversion of effector T cells into Tregs. 

Keywords

Immunology, Ophthalmology, Uveitis, Ocular inflammation

Research Area

Medical Sciences

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