A $150,000 research grant awarded by the National
Psoriasis Foundation earlier this year has helped lead
researchers to a breakthough in the understanding of how
the immune system may trigger psoriasis.
The Psoriasis Foundation
awarded the grant
to Tasha Sims, Ph.D., a
research associate at New
York University’s Skirball
Institute of Biomolecular
Medicine.
Sims researches how new
psoriasis drugs work by
depleting and altering
overactive T cells, a type of
immune system
cell. While the
depletion and alteration of T cells may stop the
cycle that leads to psoriasis, it may also turn off
other parts of the immune system that protect
against disease or infection.
Sims has been exploring the role of LFA-1 in
psoriasis. LFA-1 is part of what is called the
“immune synapse,” the organization of proteins
at the contact point between T cells and antigen
presenting cells. In psoriasis, antigen presenting
cells behave as if the body needs to fight off an
infection, and they begin overstimulating T
cells, which normally do help fight off foreign
invaders like bacteria or viruses. The T cells also
release other proteins called cytokines, which
triggers the overproduction of skin cells and the
formation of lesions on the skin surface.
In a recent article in Science, Sims and colleagues describe
how proteins on the surface of T cells and antigen presenting
cells organize and interact at the point of contact.
The structure of the proteins allows messages to be passed
between the cells—in other words, the immunological
synapse “turns on” or “turns off ” the T cell.
“These experiments will provide critical missing information
for psoriasis treatment,” Sims says.
Sims and her colleagues hypothesize that T cells with LFA-
1 blocked from playing its role in the immune synapse will
be less able to move, communicate and survive. If this is
the case, the research may aid in the development of treatments
that disable overactive T cells in psoriasis without
affecting the entire immune system. |
