Cytokines: Molecular Movers and Shakers
December 17th, 2007 by The Doc
They’re called cytokines (cyto, meaning cell, and kine, meaning movement or pertaining to motion), those molecular messengers that our immune cells use to communicate with each other. Think of cytokines as messages in bottles, cast from cellular ships into a sea of plasma, to be plucked up by other ships as they pass by. There are many different cytokines. Some people are familiar with one of them—interferon—because of its use in the treatment of Hepatitis C. Others, such as interleukin-2 (used intravenously in the treatment of certain cancers) are less well known. Still others are just being recognized by the scientific community.
In general, cytokines are produced by white blood cells in response to some perceived threat. As the cytokines are released into the circulation, they are assimilated by other cells, which interpret the molecular messages carried by the cytokines. At that point (depending on the function of the receiving cells), a cascade of immune responses is set in motion. Some cytokines attract specialized white cells to bolster the local immune response in a problem area. Others stimulate distant cells to make their own cytokines, which are then passed to still more cells, and so on. Antibody production—the task of mature B cells—is the end result of a process that includes stimulation by cytokines.
Cytokines are also important in another critical function of the immune system: recognizing self from non-self. Our immune system must be able to deal with foreign invaders without attacking the cells that make up our bodies. When this ability to identify “self” fails, we develop autoimmunity, and a plethora of illnesses can result: rheumatoid arthritis, lupus, inflammatory bowel diseases, scleroderma, thyroiditis, and so on.
Among cytokines, a group of molecules called transfer factors possess unique properties. Unlike many cytokines, transfer factors are not species specific. This means that transfer factors from one species can affect the immune response in a different species. This may be due, in part, to transfer factors’ small molecular size, a property that might also be responsible for the fact that transfer factors taken orally are still effective; other cytokines currently used therapeutically must be administered via injection.
Discovered in 1949 by Dr. Sherwood Lawrence, transfer factors have been the subject of extensive research. Since Lawrence’s day, we have learned a good deal about this class of molecules:
1. When a new threat is encountered by a naïve immune system, transfer factors are integral in the immediate activation of the immune response, thus avoiding delay that might allow the invader to gain an insurmountable foothold.
2. Once a threat has been neutralized, transfer factors serve to “down-regulate”, or modulate, the immune response, thus helping to prevent autoimmunity.
3. Transfer factors serve as part of the “immune memory,” thus affording antigen-specific recognition that allows quick response when a previously encountered threat returns. Immune memory is what allows us to quickly suppress an infection like chickenpox, for example, after our first exposure to the virus.
A good deal is yet to be learned about this class of molecules called cytokines. Several of them have gained acceptance in the treatment of certain illnesses and, as our knowledge grows, more applications will certainly be forthcoming. One intriguing aspect of cytokine research is the “fever effect” that has been described in a number of autistic children. Investigators postulate that cytokines produced in response to fever are responsible for some autistic individuals “waking up” when they are ill. Once the illness passes and the fever subsides, the children return to their previous state. Scientists are working to identify the cytokine(s) responsible for this effect. Interestingly, some parents who have given transfer factors to their autistic children have reported improvement in the children’s conditions. Though anecdotal, these testimonials raise a litany of questions about transfer factors’ role, if any, in this most troubling of conditions.
Much remains beyond the horizon, simply awaiting discovery. In the meantime, transfer factors are currently available for human consumption. Whether they possess any utility—given the dogmatic dispositions of Western medicine and the FDA—is left for the consumer to decide.
Immune Cross Reaction Theory for Myathenia Gravis and RA caused by Herpes
“The cause of autoimmune diseases is unknown, but it appears that there is an inherited predisposition to develop autoimmune disease in many cases. In a few types of autoimmune disease (such as rheumatic fever), a bacteria or virus triggers an immune response, and the antibodies or T-cells attack normal cells because they have some part of their structure that resembles a part of the structure of the infecting microorganism.”
I suspect that the Zoster Virus immune response sets in motion an autoimmune response that triggers symptoms of RA and MG. My right drooping eyelid began concurrently with a herpes simplex sore in the right roof of my mouth, caused by a burn wound initially. I progressively got RA in my right pelvis so intense that I was unable to stand or walk for months. The MG caused double vision, then difficulty swallowing and migrated to the left eye. I then got Zoster on the left side. The progression of the disease intensified over a 8 month period until I finally self diagnosed. This is what happens when you are self insured I guess.
A study seems to suggest that this is the case with a Autoimmune hepatitis.
“Autoimmune hepatitis (AIH) is a chronic disease of unknown etiology that is characterized by the presence of circulatory autoantibodies and inflammatory changes in liver histology[1]. Several triggers for AIH, particularly drugs and viral hepatitis, have been described, which may induce the development of autoimmunity in predisposed individuals[1,2]. We report a case of severe AIH preceded by varicella zoster virus (VZV) infection, which we believe, triggered the AIH. The possible pathogenic mechanism is based on the molecular mimicry hypothesis, in which viral proteins that are similar to the amino acid chains of autoantigens in the liver induce immune cross reactions that cause liver damage[3]. As far as we are aware, VZV-induced AIH has not been reported previously.” (World J Gastroenterol. 2009 February 28; 15(8): 1004–1006.
Published online 2009 February 28. doi: 10.3748/wjg.15.1004.
Copyright ©2009 The WJG Press and Baishideng. All rights reserved.
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