Autoimmune Disease

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When the Body Attacks Itself by Anne Underwood | Dec 08 '03 Newsweek
The immune system is a thing of beauty - subtle enough to distinguish dangerous invaders like viruses from benign interlopers such as food; clever enough to recognize when the body's supposedly friendly cells turn cancerous and should be eliminated. But the immune system can also go seriously awry. When it begins mauling healthy tissues, the result can be any one of 80 autoimmune diseases such as lupus or rheumatoid arthritis. "It's the price we pay for having such a dynamic, finely balanced system," says immunobiologist Jeffrey Bluestone, director of the Immune Tolerance Network at the University of California, San Francisco.

Must we limit ourselves to treating the symptoms of these disorders, or could we modulate the immune system itself? Immunologist Marc Feldmann and rheumatologist Ravinder Maini of Imperial College London posed that very question in the mid-1980s. Doctors scoffed. But three drugs for rheumatoid arthritis emerged from their research, and the same drugs are also proving useful for conditions like Crohn's disease and juvenile arthritis. This year Maini and Feldmann won the Lasker Award for clinical medical research. And some of their colleagues are talking Nobel Prize.

Drug companies are eager to expand this approach into therapies for other autoimmune diseases, which have been on the increase since the 1950s, but have few good treatments available today. Translating principle into practice will not be easy, however. The immune system is a vast network with a bewildering array of warrior - from antibody - making B cells to various kinds of T cells that can enhance antibody production, kill virus-infected cells, initiate inflammation and finally shut down and immune attack. B cells and T cells also make more than 100 types of helpers called cytokines that assist in orchestrating every aspect of the immune assault.

Maini and Feldmann zeroed in on one such cytokine called tumore necrosis factor (TNF). It derives its name fro its ability to kill cancer cells, but in excess it also initiates the inflammation of rheumatoid arthritis. In a small clinical trial, they tested and anti-TNF antibody in 20 patients who had failed to respond to other treatments. Within hours, the recipients started feeling better. In six weeks, they were climbing stairs and even golfing. Today there are three TNF blockers on the market for rheumatoid arthritis - Remicade (which Maini and Feldmann used), Enbrel and Humira.

But not all patients with rheumatoid arthritis respond to these costly TNF blockers - nor does anti-TNF therapy hold the master key to all autoimmune diseases. "There may be some therapies that are broadly applicable across a wide range of disorders, and other that are particular to one disease," says Bluestone. So doctors are targeting other immune-system components, like B cells and T cells, in an attempto to tame various autoimmune problems. Genentech's drug Rituxan, a bioengineered antibody against B cells, is now in early trials for lupus, the most challenging of all autoimmune diseases because it affects not just ne type of tissue, but organs throughout the body.

Muzzling the immune system's pit bulls is only oe approach to treating immune disorders. Another - in theory at least - is to boost the components of the immune system that naturally rein in attacks. Last month immunologist Nathan Karin at the Technion-Israel Institute of Technology in Haifa published a paper showing that the immune system makes its own anti-TNF antibodies - but only when it's also producing a lot of TNF. Karin detected antibodies in patients with rheumatoid arthritis, but not osteoarthritis (a degenerative disease), nor in normal, healthy people. "If we could harness these antibodies," he says, "we might be able to teach the body to amplify its own beneficial response."

In the long run, however, the goal of doctors (if not drug companies) is to learn to retrain the immune system so that it no longer needs drugs to make it behave. Sound impossible? "I've staked my whole career on it," says Bluestone. Several years ago he developed a bioengineered antibody to treat type 1 diabetes. The antibody latches onto the T cells that destroy insulin-producing beta cells in the pancreas. In the process, it blocks one of the crucial receptors on the T cells that is needed to activate an attack.

Together with Dr. Kevan Herold of Columbia University, Bluestone has tested the antibody in 23 newly diagnosed patients. Two years later, those who received just two weeks of treatment at the outset are making twice as much insulin as patients who didn't receive the antibodies. Bluestone notes that the effect is starting to wear off, and the participants may need booster shots. But, he adds, "what's really exciting is that the T cells seem to remain in the pancreas and retrain other T cells."

Unfortunately, even if it works perfectly, the antibody is not a cure. By the time type 1 diabetes is diagnosed, the pancreas has lost 80 to 90 percent of its insulin-making ability. That's why the ideal time to treat autoimmune disease is early on, before irreversible damage has been done. Beginning next year, the Dinora Trial will test Remicade in patients who have had symptoms of rheumatoid arthritis for no longer than 12 weeks. The goal is long-term remission. Other doctors are trying to uncover ways of testing for autoimmune diseases before symptoms even emerge. They have their work cut out for them.

Newsweek U.S. Edition

How Transfer Factor works on Autoimmune Conditions?

Autoimmune Hepatitis - Autoimmune hepatitis has a prevalence of 1-2 per 1000.  Liver enzymes are elevated, as is bilirubin. Autoimmune Hepatitis can progress to cirrhosis.  The diagnosis of autoimmune Hepatitis is best achieved with a combination of clinical and laboratory findings.

Autoimmune Neutropenia - Neutropenia is the abnormally small number of neutrophil cells in the blood.  The body identifies the neutrophils as foreign bodies and makes antibodies to destroy them thus attacking itself (autoimmune).

Graves Disease - Graves disease is a form of thyroiditis, an autoimmune disorder that stimulates the thyroid gland, being the most common cause of hyperthyroidism (overactivity of the thyroid).

Hashimoto's Disease - Hashimoto's thyroiditis is the most common form of thyroiditis, an autoimmune disease where the body's own antibodies fight the cells of the thyroid. It is named after the Japanese physician, Hakaru Hashimoto, who first described it in 1912. It is ten times more common among women than men, and runs in families.

Hyperthyroidism | Hyperthyroid - Major clinical features of Hyperthyroidism in humans are weight loss, fatigue, weakness, hyperactivity, irritability, apathy, depression, polyuria and sweating. As to other autoimmune disorders related with thyrotoxicosis, an association between thyroid disease and myasthenia gravis has well been recognised.

Multiple Sclerosis - Multiple sclerosis (MS) is a demyelinating disease, a non-contagious chronic autoimmune disorder of the central nervous system which can present with a variety of neurological symptoms occurring in attacks or slowly progressing over time. It has no cure yet and the exact cause remains unknown.

Myasthenia Gravis - Myasthenia Gravis (MG) is a chronic neuromuscular autoimmune disease that manifests itself by varying weakness of the voluntary muscles of the body. Myasthenia Gravis may affect any muscle that is under voluntary control, and certain muscles are more often involved.

Pernicious Anemia - Pernicious anemia is an autoimmune condition where the body lacks intrinsic factor, required to absorb vitamin B12 from food.

Rheumatoid Arthritis - Rheumatoid arthritis (RA) is a chronic, inflammatory autoimmune disorder that causes the immune system to attack the joints.  The symptoms that distinguish rheumatoid arthritis are inflammation and soft-tissue swelling of many joints at the same time (polyarthritis).

Psoriasis - Psoriasis is a disease whose main symptom is gray or silvery flaky patches on the skin which are red and inflamed underneath when scratched.  Psoriasis is autoimmune in origin, and is not contagious.

Psoriatic Arthritis - Psoriatic arthritis is a type of inflammatory arthritis that affects around 20% of people suffering from the chronic skin condition Psoriasis.  Psoriatic arthritis can develop at any age, however on average it tends to appear about 10 years after the first signs of psoriasis.

Systemic Lupus Erythematosus - Systemic lupus erythematosus is an age- and gender-associated autoimmune disorder. Previous studies suggested that defects in the hypothalamic/pituitary axis contributed to systemic lupus erythematosus disease progression which could also involve growth hormone, insulin-like growth factor-1 and somatostatin function.

Type1 (Insulin-dependent) Diabetes Mellitus - Type 1 diabetes is most commonly diagnosed diabetes in children and adolescents, but can occur in adults as well. It is an autoimmune disorder, in which the body's own immune system attacks the beta cells in the Islets of Langerhans of the pancreas, destroying them or damaging them sufficiently to reduce insulin production.