|
E-mail this page to a friend!
Discovery Could Lead to Treatment of Macular
Degeneration
June 21, 2005 – Scientists say they have discovered
a protein – F4/80 – may play a role in the regulation of the immune
response and protect delicate tissues that cannot survive the
“inflammation” inherent in full-blown immunity. This discovery, they
hope, can help in developing therapies for blinding eye disease, like
macular degeneration that leads to blindness in many senior citizens.
The F4/80 molecule (also known as a glycoprotein)
was first discovered two decades ago on immune cells in the eye, gut and
other privileged sites, but its function has not been understood.
“We believe that this discovery may ultimately help
in the development of therapies for blinding eye diseases such as
macular degeneration and autoimmune diseases that occur when the immune
system goes awry,” says Joan Stein-Sreilein, PhD, senior author of the
study published in the May issue of the Journal of Experimental Medicine
and senior scientist at The Schepens Eye Research Institute.
According to Stein-Streilein, the discovery is
another piece of the “immune privilege” puzzle. Certain parts of the
body, including the eyes, brain, gastrointestinal system and
reproductive system have the ability to prevent the usual immune
response onset when confronted with foreign invaders such as bacteria.
Without this special reaction, the eye’s delicate tissue would be
destroyed by inflammation and the gastrointestinal tract could not
tolerate the ingestion of food.
In an attempt to understand F4/80, Stein-Streilein
and her team have been following the immune cells (also known as antigen
presenting cells) containing the protein. In previous studies, the team
found that when these F4/80 containing cells bring antigens (foreign
substances) from the eye to the spleen, the spleen stimulates the
production of what is known as a “regulatory” T cell which stops the
immune response throughout the body as well as at the site where the
invasion took place—in this case, the eye. In a full-blown immune
response, other types of T Cells are stimulated that start the immune
attack, inflammation, and tissue destruction.
Since the F4/80 protein was identified as a crucial player in the
development of immune privilege, the Schepens’ team postulated that the
protein had an important role in immune regulation. In the current JEM
study, the team investigated mice that did not produce F4/80. They found
that the immune suppression did not occur when foreign substances were
presented to the spleen by antigen presenting cells that did not have
F4/80. “This led us to believe that the protein F4/80 had a direct role
in stopping immune response,” says Stein-Streilein.
Although the mechanism by which F4/80 stimulates
the production of immune suppressing T Cells is unknown, the team
believes that the protein may be involved in cell-cell communications.
The presence of F4/80 cells in other immune
privileged sites, such as the brain and placenta, and its exclusion from
T cell zones in the spleen suggests that F4/80 expression and immune
activation may be mutually exclusive.
According to Stein-Streilein, the next steps for
the group will be to tease out exactly how the protein accomplishes its
goal. Ultimately knowledge of the F4/80 protein and its role in immune
regulation may lead to novel therapies for autoimmune diseases of the
eye and the body.
For a copy of the article, “The macrophage F4/80
receptor is required for the induction of antigen-specific efferent
regulatory T cells in peripheral tolerance” please go to the JEM website
at http://www.jem.org/ or contact pjacobs12@comcast.net.
Schepens Eye Research Institute is an affiliate of
Harvard Medical School and the largest independent eye research
institute in the nation.
Click to More Senior News on the
Front Page
Copyright: SeniorJournal.com |
