Since interferon causes increased red blood cell destruction .. one
might think THIS is the **reason** one finds .. destroyed red blood
cells / porphyrins.. IN .. lupus .. ?

Source: Hospital for Special Surgery
Released: Sat 28-Jul-2007, 11:10 ET

New Research May Predict Who is at Risk to Develop Lupus
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Medical News   Keywords
SYSTEMIC LUPUS ERYTHEMATOSUS, SLE, AUTOIMMUNE DISEASE, INTERFERON-
ALPHA, AUTOANTIBODY
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Certain families produce higher levels of a specific molecule, called
interferon-alpha, that primes the body's immune system to turn on, and
in some cases initiate an autoimmune attack on itself, according to
new research from Hospital for Special Surgery in New York City.

Newswise - Certain families produce higher levels of a specific
molecule, called interferon-alpha, that primes the body's immune
system to turn on, and in some cases initiate an autoimmune attack on
itself, according to new research from Hospital for Special Surgery in
New York City.

Our immune system is able to defeat disease-causing viruses and
bacteria every day using chemical weapons, like interferon-alpha, that
have been honed over time. But like anything else, we can have too
much of a good thing.

Using blood samples from two large repositories, rheumatologist Mary
K. Crow, M.D., and her colleagues at Hospital for Special Surgery
compared 266 patients with systemic lupus erythematosus (SLE), an
autoimmune disease, with 405 of their healthy relatives. Specifically,
Dr. Crow, who is director of Rheumatology Research and associate chief
of the Division of Rheumatology at Hospital for Special Surgery, and
her team were looking at levels of interferon-alpha. The researchers
found that when an SLE patient had high blood levels, so did many of
their healthy first degree family members. There was a genetic link.

The study, which is now online in advance of print, will be in the
September issue of Genes and Immunity.

"There were a number of first degree relatives of patients with SLE
that had high interferon-alpha levels," says Timothy Niewold, M.D.,
first author of the study and a former rheumatology fellow at Hospital
for Special Surgery. "But otherwise, those family members looked and
felt perfectly fine. All of their diagnostics were normal."

Our immune system works by distinguishing self from non-self, so that
it preferentially attacks foreign microbes. Interferon-alpha is
normally a helpful molecule in this regard, leading the fight against
invading viruses. Genes producing high levels of interferon-alpha have
probably been selected over time to help fight infection. But high
levels of interferon-alpha in some individuals may also confuse the
immune system so that it doesn't know self from non-self anymore -
turning and attacking its own tissue as in SLE.

As far back as the 1970s, doctors had known that a characteristic of
patients with SLE, who are mainly women in their childbearing years,
was an abnormally high blood level of interferon-alpha. However, they
didn't know if the high interferon levels were the cause of the
disease or just an associated side-effect.

"A role for interferon-alpha in lupus has been suggested for a number
of years," says Dr. Crow, who is also director of the Autoimmunity and
Inflammation Research Program and co-director of the Mary Kirkland
Center for Lupus Research at Hospital for Special Surgery. "However,
all of the studies to date had focused on how the levels of interferon-
alpha were controlled and what the effects of such high levels were.
The real question was whether interferon-alpha was playing a primary
role in the disease or not."

The blood samples showed that some family members of patients with
high levels of interferon-alpha also had higher levels than unrelated
healthy individuals, irrespective of their ethnic background. This
observation supported the idea that high interferon-alpha levels play
an important primary role in the disease.

Next, the researchers examined the samples for two types of
autoantibodies common to SLE patients. SLE patients with low levels of
interferon-alpha were more likely to have neither of the
characteristic autoantibodies, while patients with the highest levels
were more likely to have both. However the healthy family members with
high interferon-alpha did not have either autoantibody. This led the
scientists to propose a "two-hit" model for the development of lupus.
Genetics that cause high levels of interferon-alpha may predispose a
person to SLE, but the disease appears only when something else,
perhaps an environmental factor, pushes the immune system to the
breaking point and causes the production of the damaging
autoantibodies.

"The high level of interferon-alpha doesn't always cause the disease,
because many healthy family members have high levels," says Dr.
Niewold, who is now an Instructor in the Section of Rheumatology at
the University of Chicago. "We think, however, that those levels
somehow prime the immune system, lowering the threshold, so that when
the wrong stimulus comes along, the cells of the immune system begin
making the autoantibodies and the person develops SLE."

The researchers are now working to identify the other players that are
involved in the progression of SLE. They hope that as they know more,
they may be able to identify those at high risk and diagnose the
condition early enough to intervene and reverse the disease.
Observational and genetic studies of families with high levels of
interferon-alpha will also help them to pinpoint the other factors,
including the relevant genetic variations that determine why one
family member develops the disease while another doesn't.

"The hope is that we may be able to use interferon-alpha levels as a
measurement to predict who might be at risk to develop this disease,"
says Dr. Crow, who is the immediate past president of the American
College of Rheumatology. "We can't do that yet, but the success of
this study is very encouraging."

Jing Hua and Thomas J.A. Lehman at the Mary Kirkland Center for Lupus
Research at Hospital for Special Surgery and John B. Harley at the
Oklahoma Medical Research Foundation in Oklahoma City also contributed
to this paper. This research was funded by the National Institutes of
Health, the Alliance for Lupus Research, the Lupus Research Institute
and the Mary Kirkland Center for Lupus Research at HSS.

About Hospital for Special Surgery
Founded in 1863, Hospital for Special Surgery (HSS) is a world leader
in orthopedics, rheumatology and rehabilitation. HSS is nationally
ranked as No. 1 in orthopedics, No. 3 in rheumatology by U.S.News &
World Report, and has received Magnet Recognition for Excellence in
Nursing Service from the American Nurses Credentialing Center. In the
2006 edition of HealthGrades' Hospital Quality in America Study, HSS
received five-star ratings for clinical excellence in its specialties.
A member of the NewYork-Presbyterian Healthcare System and an
affiliate of Weil Cornell Medical College, HSS provides orthopedic and
rheumatologic patient care at NewYork-Presbyterian Hospital at New
York Weill Cornell Medical Center. All Hospital for Special Surgery
medical staff are on the faculty of Weil Cornell Medical College. The
hospital's research division is internationally recognized as a leader
in the investigation of musculoskeletal and autoimmune diseases.
Hospital for Special Surgery is located in New York City and online at
www.hss.edu.

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