JOURACA_SP_2017

The Functions of Vg1 and Vg4 in Gamma
Delta T Cells
Katelyn Speights
The Functions of Vg1 and Vg4 in Gamma
Delta T Cells Corneal infections by herpes
simplex virus type 1 (HSV-1) can cause herpes
stromal keratitis (HSK), the leading
cause of blindness in developing countries.
Upon infection, HSV-1 triggers an immune
response that can result in corneal opacity,
scarring and eventually blindness. T cells
are critical for the immune response to HSV
-1 infection, with γδ T cells involved early
on and T helper cells later in the response.
The early response has been found to not be
harmful to the eye, while the later response
involving T helper cells is damaging and
enhances the progression of HSK. Because
of their ability to protect mice from intracorneal
infection with HSV-1, γδ T cells have
potential as a vaccine target. More specifically.
γδ T cells producing interleukin 17A
(IL-17A) represent a subset that is particularly
important for early protection from
HSV-1 infection. My project focused on
how these IL-17A-producing γδ T cells are
recruited to the cornea, and how they are
instructed to make IL-17A. We hypothesized
that corneal fibroblasts, upon infection
with HSV-1, produce the chemokine
CCL20 that serves to recruit γδ T cells
poised to make IL-17A.
Infected corneal fibroblasts also make IL-1
and IL-23, that we hypothesize provide the
requisite signals to turn on IL-17A productionin
γδ T cells. To begin testing these
Department of Biomedical Sciences
Mentor: Robert A. Barrington
hypothesis, I evaluated CCL20, IL-1 and IL
-23 production in HSV-1 infected fibroblasts
in vitro. I established cultures of murine
kidney and corneal fibroblasts that
could be maintained for up to 6 passages. At
passage 4, the cells were seeded onto tissue
culture plates and infected with HSV-1. Cell
supernatants and lysates from these cultures
were collected at 0, 6, 12, 18 and 24 hours
following HSV-1 infection and examined
for CCL20, IL-1 and IL-23 by enzymelinked
immunosorbent assay (ELISA).
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