An aspect of immunity involves the function of B lymphocytes (or B cells) that secrete antibodies. A protein expressed on B cells and other immune cells (CD40) is crucial for normal B cell action. CD40 interacts with a protein (CD40L) present on T cells that also contributes to B cell stimulation. This CD40-CD40L interaction is important for normal immune function. However, exaggerated B-cell responses to CD40 occur in autoimmune diseases such as multiple sclerosis. It has been shown that B cells from patients with relapsing-remitting multiple sclerosis (RRMS) are stimulated by CD40 to multiply significantly more than in healthy patients.
The Epstein-Barr virus (EBV) is a common virus that is found all over the world and can cause mononucleosis and other diseases in people with compromised immune systems. The John Cunningham virus (JC virus) is another common virus with up to 90% of adults in the U.S carrying the virus. However, most do not have any symptoms or illnesses with the virus, but those with suppressed immune systems (people with AIDS or taking immunosuppressive medications) can develop illnesses due to the JC virus.
Depleting B cells improves outcomes for multiple sclerosis patients, but what is the underlying biology? Peripheral blood from HemaCare helped provide answers.
Multiple sclerosis is a disease in which the protective myelin coat of nerve cells in the brain and spinal cord become damaged. Consequently, any function related to the central nervous system can be adversely affected, but the most common symptoms are severe fatigue, visual problems, altered sensitivity, and reduced mobility. The root cause of multiple sclerosis is still unknown, but the research community has learned that it is an abnormal immune-mediated response that attacks the myelin coating.
Researchers find that Nr4a1 expression in macrophages link the sympathetic and immune systems and limit inflammation during multiple sclerosis.
It is becoming more apparent every day that the different systems of the human body influence each other substantially more than what was previously thought. New research provides evidence that this is the case with the immune and sympathetic nervous systems. The linking factor is macrophages and a transcription factor they express, Nr4a1, and the result is affecting the outcome of multiple sclerosis.
Although glatiramer acetate has been around for about 20 years, we still do not have the full picture of its mode of action, especially on B cells.