what is "autoimmune"?
815190
Ordinarily, the body can distinguish between what in a normal substance and what is foreign.  In an autoimmune response, the body attacks it's own normal tissue.  Various illnesses are considered to be caused by this reaction, including rheumatoid arthritis, multiple sclerosis, lupus and scleroderma.  I suggest that you use google or another search engine to check into a specific condicion.
424980
Great question - there is intense scientific interest in this issue, however the answer is unknown.  \n\nDiabetes is an disease in which the body fails to regulate blood glucose.  Often, Beta cells (located in the pancreas) fail to produce insulin, a hormone that is required for this process.  This can be caused by dysfunction of the beta cells, but more commonly it is the result of an autoimmune disease where the body's own T cells destroy the beta cells.  Normally, the body regulates the activity of self-reactive T cells to prevent this sort of outcome, so the defect in diabetes and other auto-immune diseases is most likely at the level of regulation, not activity, of these T cells.\n\nRecent scientific data indicates that CD4+CD25+ T regulatory cells (T-regs) are an important component of the body's natural immune dampening mechanism, and these cells appear to be essential for limiting auto-immunity in several mouse models as well as in human disease.  The mechanisms of Treg function are only now becoming understood, and include expression of surface CTLA4 and secretion of TGF-beta and IL-10 - each of which seems to dampen CD8 T cell cytolytic activities.  Which of these functions is required in general for Treg activity, or for the case of diabetes specifically, is not known.  Based on current understanding, it is likely that the inability of CD4+ Tregs to control self-reactive CD8 T cells is a major factor involved in diabetes and other auto-immune syndromes.
177972
try these links. they are a quite a helpful read. \n\nwww.merck.com/mrkshared/ mmanual/section11/chapter143/143c.jsp\n\nwww.pnas.org/cgi/content/full/102/2/419\n\nwww.autoimmuneinc.com/R_and_D/tech.html\n\nwww.sciencemag.org/cgi/content/figsonly/309/5739/1380\n\ngood luck and have fun!!!
102774
Rheumatic fever is an autoimmune disease which occurs after an untreated Group A streptococcal infection, typically a throat infection. The antibodies formed against the bacteria attack parts of the body, typically the joints and the heart.\n\nGroup A Streptococcus pyogenes has a cell wall that is composed of branched polymers which sometimes contain "M proteins" which are highly antigenic. The antibodies formed against these proteins sometimes cross-react with normal tissue causing damage. Depending on the site of damage, this can lead to the clinical symptoms described in the attached article.
895535
Antigens were originally defined as non-self molecules which bound specifically to antibodies. In practice, the term antigen is used to mean any molecule recognized by the immune system. \n\nAntigens which induce adaptive immunity are called immunogens. All immunogens are antigens, and are usually called antigens unless their ability to induce an immune response is being discussed. Some antigens, called haptens, are not immunogenic unless they are covalently linked to immunogenic carriers (usually proteins). Haptens can bind antibodies once the antibodies are produced, but haptens will not induce antibody synthesis on their own. Small non-protein organic molecules, for example the antibiotic penicillin, are haptens.\n\nImmunogenicity is influenced by \n\nthe chemical nature of the antigen. \nthe antigen's size. \nthe antigen's usual presence in the body. \nantigen dose and route and timing of administration. \nwhether the antigen is easily phagocytosed. \nwhether antigen is efficiently presented to T cells on MHC. \nthe maturity of the immune system and specific lymphocytes. \nNote that immunogenicity depends on the immune system as well as on the antigen. \n\nImmunogenicity is generally higher for proteins than for other organic molecules. Protein antigens, which are the predominant sort that activate helper T cells, consequently induce more B cell antibody production, synthesis of IgG or IgA, and generation of memory B and T cells. T-independent antigens, which activate only B cells, induce IgM synthesis but not other adaptive immune responses.\n\nImmunogenicity increases with molecular size and complexity. Haptens are generally non-proteins or they are too small to be immunogenic unless they are covalently attached to a carrier protein molecule. Some carbohydrate antigens can stimulate B cells to secrete IgM in the absence of T cell help but do not elicit IgG or memory cells. Human infants make poor responses to carbohydrate antigens, so early vaccinations with bacterial polysaccharide antigens employ protein carriers. Aggregated proteins are easily phagocytosed and more immunogenic than soluble proteins. Adjuvants, including bacterial products, alum, or oil emulsification of antigen, attract and activate antigen-presenting cells (dendritic cells and macrophages) and slow antigen release to prolong exposure and improve immunogenicity.\n\nEach part of the antigen bound by a unique antibody is called an epitope. Most proteins have several epitopes that are recognized by different B cells and induce a polyclonal antibody response. In a polyclonal response, several clones of B cells each make different antibodies, all able to bind to the same antigen but at different epitopes. Epitopes may be shared by closely related antigens (cross-reactivity), so that antibody made to tetanus toxoid binds tetanus toxin. A protein epitope may be a linear sequence of amino acids or it may be assembled by protein folding. Epitopes with definite three-dimensional shapes and charged amino acids are particularly well recognized by antibodies. External membrane and cell wall molecules, often present in many copies on the pathogen, are common B cell antigens. A small peptide of 4-6 amino acids could fit into an antibody binding site, but larger proteins have more extended epitopes across their surfaces.\n\nActive immunity is induced by exposure to antigen. Antigen dose and the route and timing of antigen contact, as well as immunogenicity, influence the magnitude and nature of the immune response. Very high or very low doses of antigen induce tolerance, the inability to respond to that antigen, while intermediate doses induce immunity. We are generally tolerant to cell-bound and soluble antigens present in our own bodies. Oral tolerance to foods is common, although some foods induce allergic reactions. \n\nAntigens encountered in body tissues through subcutaneous or intramuscular injection are carried by lymph and macrophages into the lymph
573717
cancer is an auto-immune disease and can be reversed with\nproper cell to cell communication or glycosylation. the \nimmune system kills off cancerous cells. all you need are \nglyconutrients. send me and email for more info.
1119606
Altogether there are about 80 recognized autoimmune diseases, including including myasthenia gravis. Like other autoimmune diseases, myasthenia gravis can go into remission temporarily, sometimes for long periods of time.\n\nAll of these diseases develop when the immune system mistakes the body's own tissues as a threat to health and begins producing antibodies to attack them. What distinguishes one disease from another is the target.\n\nBecause autoimmune diseases tend to flare up and subside in response to emotional ups and downs, it's often recommended to experiment with some type of mind/body treatment – hypnosis, psychotherapy and guided imagery therapy. Chinese and Ayurvedic medicine are also worth exploring. The following measures are worth trying for anyone with an autoimmune disorder:\n\nDecrease protein intake toward 10 percent of daily calories; replace animal protein as much as possible with plant protein. \n\nEliminate milk and milk products, substituting other calcium sources. \n\nEat more fruits and vegetables regularly and make sure that they are organically grown. \n\nEliminate polyunsaturated vegetable oils, margarine, vegetable shortening, all partially hydrogenated oils, and all foods (such as deep-fried foods) that might contain trans-fatty acids. Use extra-virgin olive oil as your main fat. \n\nIncrease your intake of omega-3 fatty acids. \n\nTake ginger (start with one capsule twice a day). Turmeric can also be helpful. Try "Turmeric Force" capsules from New Chapter and follow the dosage directions on the package.\n\n\n\nA whole third of patients improve without treatment, particularly early in the course of the disease.\n\nMyasthenia gravis can be controlled with medications but must be used with careful medical followup because they may cause major side effects.\n\nSurgically removing the thymus gland (which often is abnormal in myasthenia gravis patients), improves symptoms in some and may completely cures others.\n\nAnother therapy offered is plasmapheresis (removing abnormal antibodies from the blood)
1140913
well actually the words are similar but they really describe different things entirely.  immunopathology can be a word describing the pathology - process of the immune system.. - this typically entails the disease process or the functioning of the system.  Autoimmunity really describes a process where the immune system is triggered and begins to attack the body or cells in the body that it wouldn't normally attack.  Scientists don't know whay this occurs, but Multiple Sclerosis is an autoimmune disease, and so is Lupus and there are others..  so one is about studing this disease process and the other is about the actual disease.. Hope this helps.
597922
In either case it is a autoimmune disease and there are certain things that can be done to stop its progress and make life easier.
755619
i am a type 1 diabetic since the age of 4...i developed hypo thyroidism also, but only after 20 years...there is some belief that type 1 diabetes develops after having an illness because your immune system has been figting to rid the body of the infection and somewhere the wires got crossed and it attacked the pancreas too...but yes, those are both auto immune diseases..
99704
I would say check with an Immunologist. Also, theres a new magazine for people with Immune deficiences.\n\nwww.igliving.com
637126
See in\nhttp://www.biosophia4jrf.com/volume_i.htm\nAllophenic mice (embryo aggregation mouse chimeras) enable us to dissect the process of spontaneous autoimmunity under physiological conditions.\nhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7997856&dopt=Abstract
201895
Actually the cause of myasthenia gravis of course like most autoimmune diseases is unknown. There may be a slight chance for surrounding the very cause to be genetic. And most cases are usually best defined with the Thymoma. But you said the patient has CML... The sternum is well known to be part of the hematopoietic function and I am thinking what is the thymus is some how affected or inflicted with a gene from the CML site. Then there is a well connected possibility with the cause of the MG. Imatinib may also be a cause of autoantibodies but for it to be greatly specific is a very rare possibility
900880
No it isnt...it is an auto immune disease whee the body attacks itself.\nSee link below for detailed info on it
275685
There are plenty of autoimmune conditions that can affect young children.  Acquired conditions like Lyme disease mentioned above, as well as chronic diseases like juvenile rhemuatoid arthritis (JRA) are two examples.  Here is the link to some info about JRA: \n\nhttp://kidshealth.org/parent/medical/arthritis/jra.html\n\nI do not mean to suggest that JRA is at fault here...it is merely one of many possibilities.  In any case, I would have the child see a pediatric rheumatologist, who deal with myriad of similar symptoms. No harm in that really, and it would help, I think.
644538
ANA Anti-nucleus antibodies) is a parameter for a group of Auto -antibodies that go against the cell core (nucleus) what results in the disturbances of the cell-functions. it is usually done when you (the doctor) suspects rheumatoid diseases, but there are usually more antibodies to be determined to tell what you are suffering from. \nA titer of the indirect Immunofluoroscence assay of 1:80 to 1:160 is considered positive. roughly sid the put your blood(serum) in a tube, added some auto-antibody-antibodies and looked for a reaction which shows itself in agglutination of the antibodies ( made visible with the before mentioned Fluorescence). \na positive result COULD mean systematic Lupus erythematodes, Lupus erythematodes of the skin, systematic sclerosis, Poly or Dermatomyositis, Sjoergen Syndrome, Myasthenia gravis, chronic-active Hepatitis, rheumatoid Arthritis and many other rheumatic Diseases. \n\nresults in this Assay vary strongly between laboratories, many healthy people especially over 60 years old show in up to 30% of the cases a titer in their blood without being sick. \ni hope i could help you to understand a little better. But understand that this parameter by itself is not strong enough of an indicator what is wrong and where your symptoms come from.
735682
A positive ANA is one of the indicators of autoimmne disease. I have lupus and lots of us have a positive ANA, but not all of us. The ANA can vary from test to test. Other conditions can cause a positive result. There are times when there will be a negative result but disease is still present. \n\nAn antinuclear antibody test in itself does not result in a diagnosis. An experience doctor, most likely a rheumatologist, is your best bet.