User:Matthew Chien/Sandbox 1: Difference between revisions

A variety of diseases have been tied to an overabundance and lack of C1q in a person's body, most of which involve the presence of anti-C1q autoantibodies. Anti-C1q autoantibodies are antibodies that target one's own C1q, specifically the collagen-like tail of C1q. These are mistakenly generated through a misdirected immune response, and have the potential to develop into an autoimmune disease, although tests have shown that as much as 2-8% of healthy individuals still contain this antibody. Low levels of C1q and the presence of anti-C1q autoantibodies has been correlated with Hypocomplementemic Urticarial Vasculitis Syndrome (HUVS) or McDuffie syndrome. The main symptoms of this disease are chronic urticarial vasculitic lesions that persist more than 24 hours or are recurring. When these autoantibodies complex with C1q, they cause serum precipitins that contribute to swelling of the blood vessels. This can further lead to organ malfunction, various inflammatory diseases, arthritis, and a plethora of other diseases. <ref>PMID:23717311</ref><ref>PMID:22328958</ref><ref>PMID:29114186</ref>

Another disease associated with the presence of anti-C1q autoantibodies is Systemic Lupus Erythematosus (SLE), or just simply lupus. SLE is a disease where the body's own antibodies attack healthy tissue and cause inflammation. This disease, in the cause of SLE caused specifically by anti-C1q autoantibodies, is seen to cause Proliferative Lupus Nephritis (LN), a type of glomerulonephritis, which is inflammation and damage to the kidneys. This causes scarring of the tissue and malfunction of the blood vessels within the kidney and ultimately lead to kidney failure if not treated properly. Studies have been preformed that show that the presence of autoantibodies, including anti-C1q, in the kidneys is capable of producing limited disposition of the kidneys but not nephritis. Only when these anti-C1q autoantibodies are presented with C1q-containing immune complexes do they cause LN. It is unknown why anti-C1q autoantibodies predominantly enhance tissue damage in the kidneys and not in other tissues known to contain C1q immune complexes. <ref>PMID:27252264</ref>

An overabundance of C1q has shown to correlate with the development of neurodegenerative diseases and loss of cognitive function. Higher age groups are seen to have larger levels of C1q, especially in their brain. This buildup mainly occurs because of poorer activity in synaptic clearing of C1q bound to neuronal RNA-binding proteins called neuronal ribonucleoprotein complexes, affecting protein homeostasis in the brain and decreasing cognitive function. C1q is involved in pruning synapses in developing brains by tagging the synapses for phagocytosis by microglia. Elevated concentrations of C1q in the synapses has been correlated with overactivity of microglia when provoked by brain injury or a series of strokes. Most cells in the body have complement inhibiting agents to regulate complement activity, whereas nerve cells lack these complement inhibitors. Astrocytes are known to secrete C1q when provoked by infections or damage to the central nervous system, and an overproduction of these can lead to over inflammation in the brain by the complement cascade and synapses loss, both fundamental components of Alzheimer's disease and various other neurodegenerative diseases. <ref>PMID: