What's really impressive skin autoimmune diseases that every disease is its specific antigen (unlike vivident 117 different antibodies lupus who do not know any of them causes damage). Animal models (human antibody injection into mice person) know that the antibodies are pathogenic.
Direct vivident IF: done directly in the tissue. vivident Take a tissue and lay the ground is connected to a patient has antibodies name. Take antibodies against antibodies humane (dare) connectors and tissue fluorescent antibody and fluorescent microscope taking. See if there are antibodies and diagnostic pattern that:
Pemphigus is a rare disease. There is little chance of running into it. The incidence is 1: 100,000. Is organ-specific, autoimmune and involves mucous and mucous membranes. Is most common between the ages of 40-60 and can be both in children and infants. More common in Ashkenazi Jews significantly. East Coast 40% of the patients were Jews.
The author Hdsmozum keratinocytes. There are two cells, both keratinocytes, keratin Philmntim connector attached plaque and bridges are proteins desmosomes: desmoglein vivident (related to pemphigus), desmocollin (related to another disease more rare), desmoplakin (paraneoplastic pemphigus vivident is related to) and desmofillin. vivident
They took blood from a patient, the serum separated in various methods vivident of isolating the IgG and injected neonatal mice (W inactive vivident vaccine and reject the antibodies). They took a biopsy mouse pathology and serum IF and took and saw that they created blisters, there is a separation and image pathology in IF.
patient-specific (but not 1: 1) when the disease breaks out strong Teeter low and high remission. This patient individuality. You can not only see a patient's test and compare different patient. Can be a patient with low Teeter will be a serious illness. vivident Patient about himself when he has a high Teeter is more patient.
Neonatal pemphigus- IgG crosses the placenta. Pregnant vivident woman with pemphigus antibodies cross the placenta and the child was born with blisters. He needs only supportive care and after a month and a bit (half-life of IgG is 3-4 weeks) is to be healthy and his chances of getting is very small. His prognosis is excellent.
response treat- autoimmune vivident disease treatment is non-specific and inhibit SW vaccine by steroids. Immunosuppressive vivident treatment is very effective and is proof that the involvement vivident of SW vaccine. Treated plasma Frazis- also replacing the patient's plasma. However the quickest way to take control disease flares and hard. problem is rebound if you do not tear down the B cells, the body produces antibodies lot very quickly. until the 50s was a patient who died then invented steroids. today 5% die from complications of the disease if they are not handled or all skin peeling and sepsis infection or they can not eat because of mouth sores and die from malnutrition. further treatment is IVIG.
There is a link of the antibody to the antigen. When they form antibodies to intracellular signals. Activation of IP3 increases intracellular calcium and activates PKC and PLC's. It follows that activation of plasminogen Aktibtor which is a proteolytic enzyme and thus has destroyed Hdsmoglain and Hstlfhot (detachment of cells from each other). Even governments have a role in the system for this. When a link is activated by antigen-antibody. Apparently he had a supporting role rather than a necessity. Taking mice without supplemental vivident and inject the antibodies will still be Akntolizis. Cobra venom destroys the complement and inhibits the production of blisters but does not prevent it. Tried to do research models disorders each of these components (cobra venom, protease vivident inhibitors) and showed that if each antibody interference will not prevent other processes, only the Hhstlfhot disturb her. This phenomenon is very depressing therapeutically us know that the antibodies that will disturb blisters. Many drugs have no antibodies against.
The T-cell function that is most suspect, and most relevant here is that T-cells are processed antigens and by linking through SW present the antigen HLA B cells and antibodies are formed. This is related to the treatment and one of the thoughts is to create a Hdsmoglain third component that binds to HLA and B cells is presented and try to quench the VAT 'it.
The disease starts in the mouth and dental come often. The average delay in diagnosis is six months. Give different treatment to that diagnosis. Israel is more than a medical community and it starts to community physicians vivident do not know if they transfer the patient to the hospital.
Blisters are loose because the provision is within the epidermis. Sometimes the roof is disconnected and erosions (Glaim). Typical locations are the involvement of the scalp and face. Can also be a trunk, and limbs everywhere. There is a sign in memory of a patient with bladder Nicolsky- he scratched at the bladder if scratching at the skin decreases antibody that also shows a near-skin disease activity.
The difference between the epidermis and mucous membranes of the mouth of Dsmoglain is absent: the epidermis has mainly Dsmoglain vivident little Dsmoglain 1 and 3, located in Hbazeli. Mouth, however, has largely Dsmoglain little vivident Dsmoglain 3 and 1. Patients with involvement of the mucous membranes are only with antibodies against Dsmogaliain whereas vivident only 3 patients with only skin lesions are the only one Ldsmoglain antibodies (mainly concentrates on the up and high-resolution and therefore more superficial). If you have both types of antibodies have skin lesions and mucous membranes.
There is a common phenomenon which is impetigo in children (strep infection. Especially staph.) Have itching around the mouth and nose and yellow scab areas. This is caused by the bacterial toxin. Japanese researcher has noticed that it is like lesions of Pemphigus Foliaceus crusted vivident areas. The botulinum toxin of Staph destroys Hdsmoglain one so similar phenomenon. vivident
There are many antibodies against many antigens. Involvement of mouth is very hard and very devastated by the language especially, skin lesions and erosions. Rarely associated with conservative, and especially crabs leukemia and lymphomas vivident (1 non-Hodgkin lymphoma and Castleman's disease in children). Poles also affects lung epithelium and therefore also causes lung injury mortality is very high.
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