New Animal Model Helps Scientists Understand The Emergence And Progress Of Multiple Sclerosis

Using a new animal model, scientists have gained some important new insights into the emergence and progress of multiple sclerosis (MS), a very complex disease of the nervous system.

The work done by scientists from the Max Planck Institute of Neurobiology in Martinsried and an international research team suggests that B cells play an unexpected role in the spontaneous development of the disease, and that particularly aggressive T cells are activated by different proteins.

Multiple sclerosis - Symptoms - Causes - Diagnosis - Treatment
Multiple sclerosis can be a severely disabling autoimmune disease that affects the myelin or insulating layer of the nerve fibers and typically has remissions and relapses

The researchers even say that the new animal model is helping them understand the emergence of the most common form of the disease in Germany.

According to them, there is much evidence to support the fact that MS is triggered by an autoimmune reaction: immune cells that should actually protect the body against threats like viruses, bacteria and tumors, attack the body's own brain tissue.

Even though the harmful immune reaction can be attenuated to delay the disease's progress using new treatments, serious side effects pose a major problem. This makes it imperative to develop new treatments with lesser adverse effects, something that requires better understanding of the disease.

Risk of Multiple Sclerosis Relapse Reduced by Breastfeeding
Women with multiple sclerosis who breastfeed exclusively for at least two months are less likely to experience a relapse within a year after their baby's birth

For their research, the researchers specially bred mice to develop a disease pattern that was practically identical to the course of the human form of MS most common in our part of the world.

The researchers even say that the research using the new model has already shown that the emergence of the disease requires significantly more immune cells than previously assumed.

Statins Good For Cholesterol But Bad For Multiple Sclerosis
McGill University researchers in Canada say that a treatment with high daily dosages of statins, commonly prescribed drugs that effectively reduce blood cholesterol levels, may actually

Scientists have to date carried out MS research on the assumption that the disease mainly results from attacks on a group of white blood cells known as T cells. These immune-system cells provide a kind of 'immediate response' to pathogens: they recognize the pathogens, activate the immune response and thus trigger the destruction of the harmful cells.

Besides T cells, the immune system has B cells too, which also react to the presence of a pathogen, are activated and start to divide rapidly.

Thousands of cells are created which produce a pathogen-specific antibody. An invasion of pathogens can be overcome quickly and effectively through the targeted interaction of T and B cells.

The researchers say that their new model shows that unlike the T cells, the B cells have hitherto been erroneously assigned a subordinate role in the emergence of multiple sclerosis.

They say that in the new mouse model, T cells also attack the body's own brain tissue. However, this is not sufficient to trigger the disease, as when the scientists remove the B cells, the animals remain healthy.

"This observation surprised us all because it contradicted the prevailing doctrine," notes researcher Gurumoorthy Krishnamoorthy.

According to the researcher, there must be some kind of interaction between the T and B cells, that the resulting army of B cells triggers the full-blown form disease through its antibody attacks.

The researchers believe that the insights gained through studies on the new mouse models may help develop novel treatments that should have considerably fewer side effects than the previous, rather unspecific approaches.

Reports on their work have been published in Nature Medicine and the Journal of Experimental Medicine.

Source-ANI
ARU