I am new here and have had Lupus for 20 years now and had been in remission up til last year. I know have Lupus kidney and see a specialist for that regularly. I went and seen him yesterday and he was telling about a new drug that is used in Cancer patients, but is being tested and look at real closely for Lupus patients. It is called Rituxan and it destroys all B bllod cells, which some think are a big problem for Lupus patients. This drug is used in Rematoid Arthtritis patients now. It is administered by IV and can take 10 hours to administer. It is given one 1 day and then again 15 days later and that is the only doses you would recieve. The reason for so long is due to the fact that if given to fast a person can feel as though they are having an allergic reaction. They will get cold chills, the shakes, and feel crappy. Now my doctor said that this drug is still about 2 years out for Lupus patients, but he feels that it will be used for Lupus.
To me sounds like something I would try. The only question I would have would be what other purpose are B blood cells used for? I had asked him this and we got another subject and I forgot to get my answer.
B cells develop from stem cells in the bone marrow. At the youngest stages in the bone marrow, these cells develop antigen-specific surface antibody
( IgM and IgD ). The naive B cells then enter the circulation and travel around the blood and lymphatics through tissue and lymphoid organs. The B cells are called naive because they have not seen antigen yet.
It is important to know that each and every B cell (and there are many millions in the body at any one time) has a different antibody on its surface. In addition, once a B cell makes surface IgM, it can then make a different class of antibody ( class switch ) but all the antibodies made by that cell recognize the same antigen.
In the lymph nodes, naive B cells may encounter an antigen recognized by their surface antibodies. There are many (more than 90%) that circulate their entire life span without encountering antigen. These cells die within a few days. When B cells do encounter antigen, the results are as follows:
B cell activation
B and T cell interaction
Differentiation into plasma cells
Antibody secretion and class switch
B memory cells
There are several diseases that involve antibodies and B cells (and Lupus is one of them). Selective IgA deficiency, for example, is also a common asymptomatic immunodeficiency occuring in 1/600 individuals. Fewer individuals are affected more severely by malignancies of the immune system, and of the B cell line. Leukemias and lymphomas result.
B cell receptor signaling is abnormal in patients with active systemic lupus erythematosus. Studies suggest that B cells from systemic lupus erythematosus patients display molecular signaling defects that most likely contribute to pathogenesis of the disease and explain the characteristic hyperactivity of B cells in active disease. Systemic lupus erythematosus (SLE) is a complicated autoimmune disease diagnosed on presentation of a variable subset of a wide array of clinical symptoms. The feature common to all SLE patients, however, is the presence of autoantibodies. Although self-reactive B cells produce the autoantibodies essential to the diagnosis of disease, B cells have proven in recent years to be active participants in the development of the disease, irrespective of autoantibody production. "In light of this advancement, a central question surrounding the pathogenesis of the disease is whether intrinsic defects in SLE B cells play a role in triggering the immunological events that result in the onset of clinical disease. Although other immune cells play a role in SLE, B cells from SLE patients display signaling defects that may underlie pathogenesis and explain the characteristic hyperactivity of B cells in active disease. This article will present the current understanding of how B cell signaling plays a role in the pathogenesis and exacerbation of disease in human SLE."
I hope that this has answered you question
Peace and Blessings