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Infusion Nursing Notes by Nufactor provides education, resources and support to promote successful patient therapy within the infusion nursing community.

Monoclonal Antibodies: How do They Work in Autoimmune Conditions?


By Leslie J. Vaughan, R. Ph.

Monoclonal antibodies are relatively new therapies. Initially, most monoclonal antibodies were developed to treat cancers. In recent years, the use has expanded to the treatment of autoimmune conditions.

To understand how monoclonal antibodies work, a quick review of the immune system is necessary. The immune system is comprised of multiple organs and cells. For example, the skin (an organ) is considered the first line of defense in the immune system since it acts as a barrier to keep foreign items out. The organs of the immune system include the skin, bone marrow, thymus, lymphatic system, spleen and mucosal tissue. The cells of the immune system include many of the white blood cells and other types of cells. The most critical cells relating to monoclonal antibodies are T cells, B cells and cytokines. T cells and B cells play a critical role in how the immune system learns and develops a memory. Cytokines (from the Latin cyto = cell and kinos = movement) play a key role in the communication between cells. The immune system memory is what protects individuals from exposure to infections and other immune issues. At the most basic level, T cells are important in the development of B cells. B cells learn to recognize foreign antigens, and then play a role in the development of an antibody to counteract or destroy foreign antigens. Cytokines are important in directing how the body responds to inflammation, infection and trauma. 

In some cases, something goes wrong with the immune system and it loses the ability to remember its own tissue, so the immune system sees it as foreign and begins to develop antibodies against some of its own tissues. These types of antibodies are referred to as autoantibodies. This recognition of self as foreign is the basis for many autoimmune conditions. For a more in-depth review of the immune system and how it works, visit the National Institutes of Health website at www.niaid.nih.gov/topics/immunesystem/Pages/overview.aspx.

Older therapies in the treatment of autoimmune conditions were mostly targeted toward managing symptoms, or they were very broad based in the attempt to destroy or bind cells. The development of monoclonal antibodies has led to new therapy approaches in which  treatment is focused more directly on specific cells (and functions) of the immune system. Monoclonal antibodies work by a number of mechanisms such as blocking the function of the T cell, inducing the death of B cells, or by modulating signaling pathways (cytokines), all of which help regulate the immune system.  

A monoclonal antibody works at a specific cellular level to eliminate the production of, or to bind, the faulty antibody. 

Currently, monoclonal antibodies are approved by the U.S. Food and Drug Administration to treat several autoimmune conditions. For example, Remicade, Humira, Enbrel, Actemra, Cimzia, Rituxan, Simponi and Tysabri are all monoclonal antibodies approved to treat autoimmune conditions such as rheumatoid arthritis, Crohn’s disease, ankylosing spondylitis, multiple sclerosis and others.   

As with all medications, there is the possibility of developing side effects, some of which are very serious. The risk of developing side effects should be compared with the benefit of taking the medication to control the autoimmune condition. This is known as a risk-to-benefit ratio. Patients should discuss this ration with their physician. A pharmacist may also be able to provide patients with information.

In summary, monoclonal antibodies are an emerging class of medications receiving wide attention in their utility in the treatment of autoimmune conditions. They work by interfering with specific aspects of the immune system causing the development of autoantibodies. They do have side effects, so their use should be discussed thoroughly with a physician. 

Comments (3) -

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    6/3/2015 6:13:48 AM |

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