Damping Down Diabetes

SRxA’s Word on Health was very excited to learn of some amazing new research coming out of UC San Francisco.  Scientists there have identified a new way to manipulate the immune system and keep it from attacking the body’s own molecules in autoimmune diseases such as type 1 diabetes, rheumatoid arthritis and multiple sclerosis.

More than 100 different autoimmune diseases have been discovered and they disproportionately affect women.  Of the 50 million Americans living and coping with autoimmune disease  more than 75% are women.  Autoimmune diseases are one of the top 10 leading causes of death of women under the age of 65 and are responsible for more than $100 billion in direct health care costs annually.   Crohn’s disease, ulcerative colitis, lupus, multiple sclerosis, rheumatoid arthritis, psoriasis and scleroderma by themselves account for > $50 billion.

But now, researchers, led by immunologist Mark Anderson, MD, PhD, a professor with the UCSF Diabetes Center, have discovered a type of immune cell called an extrathymic Aire-expressing cell (eTAC), which puts a damper on immune responses.  eTAC’s are a type of  dendritic cell – which make up less than 3% of the cells in the immune system. And, eTAC cells themselves account for a small fraction of all dendritic cells. eTACs reside in lymph nodes and spleen in both humans and mice.

In this study, Anderson’s team determined that eTAC’s can counteract the overactive immune response in autoimmune diseases and, in a mouse model of diabetes, can be manipulated to stop the destruction of the pancreas.

By displaying “self” molecules to T cells that target them, and permanently turning off these T cells, eTACs help the immune system tolerate the molecules naturally present within us.  “The mouse model we are working with involves using T cells that normally attack the islet cells of the pancreas, specifically by recognizing a molecule called chromagranin A that is present on islet cells,” Anderson said. “But if the eTACs can get to the T cells first and display chromagranin A, they can prevent T cells from attacking the islets.”

Anderson aims to exploit eTACs therapeutically by finding out how to grow them in large numbers outside the body. “We need to figure out how to grow a lot of these cells, to load them up with whatever molecule it is that we want to induce tolerance to, and then to load them back into a patient,” he said. “Such a strategy could help selectively shut down an unwanted immune response, such as the anti-islet immune response in type 1 diabetes.”

Dendritic cells work with T cells a bit like a sheriff working with a bloodhound.  But instead of presenting an article of clothing, dendritic cells present a specific molecule. If the molecule displayed by the dendritic cell matches the one the T cell was born to target, then that T cell would be activated to expand its numbers and to attack cells or tissues where the molecule is present.

When the interaction is between eTACs and T cells, however, the targeted T cell instead is turned off forever, and never seeks its molecular prey.

Given that the prevalence and incidence of and type 1 diabetes and other autoimmune diseases, such as Crohn’s, lupus and celiac disease are on the rise, this new research is extremely important, both from a public health and economic perspective.  With as many as three million Americans having type one diabetes and the incidence growing by more than 3% per year a cure is desperately needed.

The Scoop on Poop

What are your bowel movements telling you?

Whether you love or hate the Quilted Northern TP ads on TV,now’s the  time to get real about what happens in the bathroom. Before March morphs into April we need to spread the scoop about poop in recognition of colorectal cancer awareness month.

Bottom line, (excuse the pun), we all poop. So now it’s time to stand up, or sit down, and take notice of what our bowel movements are telling us.

Signs of everything from disease to stress may show up in your bathroom bowl. The key is knowing what to look for — and what the signs may mean.

First off, there is no normal. People are different. So are bowel movements. The size, shape and consistency of feces will change greatly from person to person.

So instead of looking for “normal,” look for change. Are you going less, or more often? Has the consistency altered? Have you gone from runny to solid? If you experience a noticeable change that lasts, it’s time to see your doctor.

Are you seeing red?

If there is blood in your feces on a recurring basis, you need to see a doctor, stat. Blood can be a sign of polyps or colorectal cancer. It also can be caused by benign conditions such as hemorrhoids and anal fissures. In any case, it’s worth getting checked out.

Also, keep an eye out for other symptoms: weight loss, fever, chills. When they come together, those are “high-alert” symptoms of bowel disorders.

Size does matter!

If you used to have sizeable stools but now they are always pencil thin and hard to pass, consult your doctor. In certain types of colorectal cancer, the bowel gets narrow, and so can your bowel movements. And while thin stools do not automatically mean cancer you should still see your doctor and have a  colonoscopy just to be on the safe side.

Consistency, consistency, consistency

We all have bouts of diarrhea from time to time, usually as a result of food poisoning or an infection. But if you have frequent diarrhea it could be a sign of an inflammatory bowel condition such as Crohn’s disease or ulcerative colitis.

The scoop on stress

Your body as well as your brain reacts to things that go on around us. The impact of stress and unresolved issues may show up in your bathroom.

So next time you go to the bathroom instead of simply wiping and flushing take a moment or two to look and learn what your bowel movements are telling you.

No s**t!

 

Unlocking the Mystery of Autoimmune Disease

A key feature of the immune system is its ability to discriminate between self and non-self.

When the mechanisms that prevent the immune system from attacking itself break down, it can result in autoimmune disorders such as multiple sclerosis, rheumatoid arthritis, Crohn’s disease and diabetes.

Now researchers at Columbia University Medical Center claim they have not only found out why people with autoimmune diseases attack their own tissues and organs, but also how to correct the problem.

According to a study just published in The Journal of Clinical Investigation scientists have identified a defect in the T cell regulatory pathway which normally controls autoreactive T cells.  The majority of people with Type 1 diabetes who were tested were found to have a defect in CD8+ T cells that impacted their recognition of a common target structure known as HLA-E/Hsp60sp. More importantly, researchers were able to successfully correct the defect in-vitro.

“For decades, autoimmune diseases have been treated by reducing overall immune response. That’s been effective in extending life spans, but has been hard on the quality of life for many of those patients,” said lead researcher Hong Jiang, M.D. Ph.D.

Current therapies for treating autoimmune disease include steroids, which systemically suppress the immune system, resulting in multiple side effects, including weight gain and increased susceptibility to infections.  Therapies based on this new research are designed to selectively suppress immune responses to self-antigens without damaging the body’s normal anti-infection and anti-tumor responses.

This research is significant. The Columbia University scientists believe that this greater understanding of the defect could eventually lead to prevention of autoimmune diseases altogether.

SRxA’s Word on Health is keeping everything crossed.