Autoimmunity Antibodies

A healthy body is armed with an effective system for resisting invasions and attacks by viruses, bacteria, or parasites. This system is called the immune system. Sometimes, the immune system malfunctions. Autoimmunity is a category of diseases in which a person’s own immune system mistakenly attacks normal cells or tissues in their own body. It is a misdirected immune response that occurs when the immune system goes amiss and attacks its own body. Autoimmunity is a condition characterized by precise responses by the immune system by a specific humoral or cell-mediated immune response. Specifically, the body’s own immune system produces antibodies in response to its own tissues or blood components. In essence, autoimmunity is the failure of a creature to recognize its own bodily cells as belonging to its own body. Sometimes, autoimmune disorders are caused by an incomplete germ development of an organism and as a result, its own immune system can react against its own cells, tissues, and organs. Autoantibodies or T lymphocytes can be seen in those suffering from autoimmune disorders and these are reactive with host antigens. Common autoimmune disorders include Grave’s disease, Guillain-Barré syndrome, and Crohn’s disease.

The anti-CILP antibody binds against the cartilage intermediate layer protein. The CILP protein is thought to play a role in the structure of cartilage. Cartilage intermediate layer protein is an antagonist of TGF-beta 1 (TGFB1) and IGF1. Over expression of cartilage intermediate layer protein (CLP) impairs chondrocyte growth and matrix repair. This protein is expressed specifically in cartilage. Defects in CILP cause intervertebral disk disease (IDD). Intervertebral disk disease occurs in vertebrates, especially dogs and cats, and is characterized by pain and neurological deficits. Intervertebral disk disease is caused by degeneration and displacement of the fibrocartilage located inside intervertebral disc. Symptoms of IDD range from minor pain, to extreme pain and paralysis. Anti-WAS or Anti-WASP antibody binds against the effector protein for Rho-type FTPases. It is also known as Wiskott Aldrich Syndrome (eczema thrombocytopenia) antibody. The target protein regulates the structure and workings of the actin cytoskeleton in the thymus and spleen. The Wiskott Aldrich Syndrome antibody target also possibly regulates lymphocytes and platelet function. Defects in WAS are the cause of Wiskott-Aldrich syndrome, thrombocytopenia type 1, and neutropenia severe congenital X-linked. WAS affected individuals suffer from eczema, a low platelet count, immune deficiency, and bloody diarrhea. Thrombocytopenia is effectively a decreased number of blood platelets which increases one’s potential for uncontrollable bleeding and reduced ability for blood clotting. Individuals affected with severe congenital neutropenia are prone to recurrent infections due to a deficiency of neutrophils. Neutrophils are a type of white blood cell that is responsible for reducing inflammation and fighting infection.