Autoimmune kidney disease

Monash researchers have solved a mystery, revealing how certain immune cells work together to instigate autoimmune kidney disease.The study, led by Professor Michael Hickey and Professor Richard Kitching from Monash University's Centre for Inflammatory Diseases. In glomerulonephritis, an immune disease of the kidney, rogue immune cells damage the kidney via a misdirected inflammatory attack.

Special cells called monocytes continuously patrol the glomeruli by crawling within its blood vessels. Monocytes are very good at 'picking up and removing rubbish' and being on the lookout for signs of infection and tissue injury. However in autoimmunity, some immune cells in the circulation are highly reactive to molecules picked up in the kidney.

Patrolling monocytes can display these molecules to the reactive immune cells in the bloodstream, resulting in the rogue cells remaining in the kidney and turning on an unnecessary and damaging inflammatory attack. This autoimmune damage to the kidney can severely impact on the normal function of the kidney, if left untreated.

 This damage occurs while the cells are moving around in the kidney blood vessels. This process, known as intravascular antigen recognition, has never been described before for the key helper T cells that direct and control the immune response.
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Bacteria in milk linked to rheumatoid arthritis

A strain of bacteria found in milk and beef may be a trigger for developing rheumatoid arthritis in people who are at risk, according to a new study from the University of Central Florida. A team of UCF College of Medicine researchers has discovered a link between rheumatoid arthritis and Mycobacterium avium subspecies paratuberculosis, known as MAP, a bacteria found in about half the cows in the United States. The bacteria can be spread to humans through the consumption of infected milk, beef and produce fertilized by cow manure.

For the study, researchers recruited 100 of her patients who volunteered clinical samples for testing. Seventy-eight percent of the patients with rheumatoid arthritis were found to have a mutation in the PTPN2/22 gene, the same genetic mutation found in Crohn's patients, and 40 percent of that number tested positive for MAP. People born with this genetic mutation and who are later exposed to MAP through consuming contaminated milk or meat from infected cattle are at a higher risk of developing rheumatoid arthritis.

Rheumatoid arthritis is an autoimmune and inflammatory disease that causes the immune system to attack a person's joints, muscles, bones and organs. Patients suffer from pain and deformities mostly in the hands and feet. It can occur at any age but the most common onset is between 40 and 60 years old and is three times more prevalent in women. Some RA patients suffer from Crohn's disease and vice versa, the researchers say a national study needs to investigate the incidence of the two diseases in the same patients.
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Effects of estrogen treatment in multiple sclerosis

A study by UCLA researchers reveals the cellular basis for how the hormone estrogen protects against damage to the central nervous system in people with multiple sclerosis (MS). The researchers found that estrogen treatment exerts positive effects on two types of cells during disease -immune cells in the brain and also cells called oligodendrocytes. Complementary actions on these two types provide protection from disease.

Multiple sclerosis is a chronic autoimmune, neurodegenerative disease marked by visual impairment, weakness and sensory loss, as well as cognitive decline. These symptoms emerge when inflammatory immune cells destroy the myelin sheath that surrounds nerve processes called axons. Loss of that protective insulation disrupts electrical communication between nerve cells. The third trimester of pregnancy has been previously shown to reduce relapse rates by approximately 70 percent as compared to before pregnancy, and other studies have shown benefit over the long term due to multiple pregnancies.

An estrogen unique to pregnancy that is made by the fetus and placenta has been proposed by Dr. Rhonda Voskuhl and colleagues to mediate this pregnancy protection in both the MS mouse model as well as in two successfully completed clinical trials of estriol treatment in MS patients. How that happens has remained a critical question. Voskuhl, who led the latest study, reported mouse studies showing that estrogen protected the brain from damage by activating a protein called estrogen receptor beta (ERb). Her new research identifies which cells within the brain are mediating this protective effect.

The researchers first genetically eliminated ERb in either immune cells of the brain or in oligodendrocytes, the cells that make the myelin sheath, as a way of making cells unresponsive to estrogen during the MS like disease in mice. They then treated mice without or with ERb in these cells to ask if disease protection was lost or not. Loss of protection during treatment meant that the treatment was acting on the cell that had the receptor removed. Results showed that the estrogen-like treatment was acting on both immune cells of the brain as well as on oligodendrocytes, together resulting in repair of myelin and less disability.

Drug developers often optimize therapies by targeting only one single cell type. By contrast, this study confirms that this estrogen-like compound can combat MS via complementary effects on two distinct cell types. Voskuhl and other UCLA researchers are in fact now developing a next-generation estrogen-like compound with robust biochemical effects on oligodendrocytes and immune cells in the brain.
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Pigment transplant for vitiligo

Vitiligo is one of the most common autoimmune skin diseases and is caused by a lack of melanin, the pigment that gives skin its colour: the body’s immune system attacks the pigment cells, mistaking them for foreign invaders. This causes painless white patches on exposed areas such as the face and fingers, although they can also appear on the wrists, around the eyes, groin, armpits and inside the mouth.

Stressful activities like childbirth, hormonal changes or skin injury may trigger it, it could also be genetic, it affects all skin types, but not visible on fair skin. There are two types of vitiligo-generalised symmetrical type: it affects both sides of the body symmetrically and segmental vitiligo which affects only one area of the body and is less likely to progress- it is more responsive to treatment because a smaller area is affected.

Presently, there is no cure for vitiligo, but some treatments can reverse pigment loss if used early. These include topical steroids-to calm inflammation, and vitamin D cream, thought to have a protective effect on melanocytes, the cells that produce pigment in skin. Other options include pimecrolimus and tacrolimus, creams that are usually used for eczema, which can repigment the skin, protecting the skin from the sun is also important, as the white areas have no pigment to protect them from ultraviolet light. The use of narrow ultraviolet B light phototherapy can be useful with protopic cream, an immunosuppressant treatment that turns off the autoimmune reaction.

The ultraviolet light stimulates the melanocytes in a similar way, melanocytes proliferate when exposed to sunlight, to darken and protect the skin against sun damage. Another option is PUVA psoralen ultraviolet A light treatment, where the patient is given a drug to make them more sensitive to light, they are then exposed to UV light twice weekly for up to two years.

 For pigment transplant, researchers prepared the skin by using either a laser or a tool to injure the vitiligo patch, making it ready for the transplanted cells, the method is suitable for patients that have vitiligo that affects only a small area and has been stable for at least six months. 1-2cm square of skin from the thigh is removed taking just a thin, superficial layer, and put this into a chemical solution. This separates the pigment cells from fibrous tissue. Harvesting the cells from the chemical solution with a syringe and apply it to the area of skin affected by vitiligo, followed by Excimer laser treatments to correct the disease.
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Autoimmunity contributes to Parkinson's disease

 Autoimmunity  is when the immune system attacks the body's own tissues. Parkinson's disease is neurodegenerative movement disorder.
Malfunctioning immune system contributes to Parkinson's disease.

Two fragments of alpha-synuclein, a protein that accumulates in the brain cells of Parkinson's disease patients can activate the T cells involved in autoimmune attacks.

Dopamine neurons that are affected by Parkinson's disease are vulnerable because they have proteins on the cell surface that help the immune system recognize foreign substances.

 Researchers examined blood samples from 67 Parkinson's disease patients and 36 healthy controls to fragments of alpha-synuclein and other proteins found in neurons.

 The immune response was associated with a common form of a gene found in the immune system, which may explain why many people with Parkinson's disease carry this gene variant.

 Immunotherapy can be used to increase the immune system's tolerance for alpha-synuclein, which could help to prevent worst condition of Parkinson's disease.

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Discovery of protein linked to many autoimmune diseases

Researchers have discovered a new method of detecting small amount of a protein known as interferon in patients.
The method shows different levels and cellular sources of diseases.

Interferon are group of signaling proteins made by host cells in response to the presence of many pathogens like virus, bacteria, tumor cells and parasites.

Wrong activation of interferon signal can cause the immune system to attack healthy tissue and cause many autoimmune diseases in the body.

Elevated interferon is associated with complex autoimmune disorder like SLE, dermatomyositis and diabetes.

Mutations in genes can also cause type 1 interferonopathies. Darragh Duffy and some researchers developed an ultra sensitive method of detecting small amount of interferon in human blood.

The researchers were able to measure interferon levels in the blood of healthy SLE, dermatomyositis and type 1 interferonopathy patients.

Interferon levels were high in patients with type 1 interferonopathies, by isolating individual types of blood cells, it was discovered that mutations in a gene known as STING can cause high production of interferon.

Omega-3s may serve as therapy for type 1 diabetes

Type 1 diabetes is an auto-immune condition that activates the immune system to destroy pancreas cell. When the cells are destroyed, pancreas cannot produce insulin.

People with type 1 diabetes depend on insulin to replace what the body cannot produce, new research discovered that omega-3 fatty acids can reduce autoimmune responses of the disease.

Omega-3 fatty acids can stop inflammatory process in the body, this process can stop or prevent autoimmune diseases.

Non-obese diabetic mice were used for an experiment, omega-3 was increased in their diet  and were tested every 3 months to detect glucose and insulin tolerance.

The researchers examined the pancreas of the mice for insulitis, they discovered that adding omega-3 to the diet of mice improved glucose metabolism and control blood sugar and insulin for 182 days and prevents autoimmunity.

Facts about Lupus

Lupus is a chronic autoimmune disease in which the body's immune system attacks it's tissues and organs.

Lupus erythematous is the most common type of lupus.

It can damage the skin, joints, brain, lungs, heart, kidneys and blood vessels.

Common symptoms are: headache, fatigue, inflammation, joints pain, memory loss and butterfly rash

It is not contagious.

It is common among women buy it can affects men and women. It can attack at any age but common between age 15 and 44.

It raises the risk of Infections, cancer and pregnancy complications.

Doctors believe that lupus results from both genetic and environmental stimuli.

Immunosuppressant is one of the treatments of lupus.

Presently, there is no cure for lupus, its symptoms can be controlled by medications.

Effects of Zika virus on your heart

Zika virus is primarily transmitted  through the bite of an infected Aedes mosquitoes. Centers for Disease Control and Prevention (CDC) has confirmed that Zika can spread through sex, infected blood during transfusion and pregnant mother to foetus.

This virus could harm the heart by damaging the  heart muscle cells or by promoting inflammation in the heart of infected people, Zika is also linked to autoimmune disorder that causes muscle weakness and paralysis.

People infected with zika virus should get enough rest, drink enough water and seek medical care, presently there is no vaccine available for zika virus.

Zika can be prevented by wearing light- coloured clothes that cover every parts of the body and sleeping inside insecticide treated mosquito net.