Treatment for type 2 hypersensitivity typically involves immunosuppressants to prevent the action of unusual antibodies. Diagnosis may involve direct immunofluorescence to help identify causative antibodies. Methods of diagnosis vary according to these subsets, as a doctor must be cautious to avoid provoking further damage.
There are different subsets of type 2 hypersensitivity, depending on the trigger and the response.
autoimmune neutropenia if the body destroys neutrophils.autoimmune hemolytic anemia if the red blood cells burst.the blood disorder immune thrombocytopenia if there are not enough platelets.This can cause long-term damage to cells and tissues, resulting in conditions such as: Type 2 hypersensitivity causes cytotoxic reactions, meaning that healthy cells die as they respond to the antigens. Additionally, type 2 can also involve IgM antibodies. The difference between them lies in the form of antigens that generate a response. In fact, type 2 and type 3 hypersensitivity both result from the same class of antibody, called IgG. Similar to type 1, type 2 hypersensitivity reactions also involve antibodies. Also, people should try to avoid the allergen in the future. Some people may require emergency medical treatment with an immediate effect, whereas people with mild symptoms may require other medications. There are different treatments for type 1 hypersensitivity, depending on the cause of the reaction and how the body responds. After this, they will conduct a physical examination in addition to blood and allergy tests to help identify which antigen caused the reaction. The first step a doctor may take to diagnose type 1 hypersensitivity is assessing the person’s history, including taking information on signs and symptoms and reviewing their medical records. Some physical symptoms of type 1 hypersensitivity can include: As the body now recognizes the antigen, it is able to produce a response that results in the symptoms that people typically experience with an allergic reaction. During the effect stage, the person has exposure to the antigen again. There are two stages to type 1 hypersensitivity: the sensitization stage and the effect stage.ĭuring the sensitization stage, the person encounters the antigen but does not experience any symptoms. allergic conditions, such as allergic rhinitis, allergic asthma, and conjunctivitis.environmental sources, such as mold, latex, and dust.animal sources, such as cats, rats, or bee stings.food products, such as nuts, shellfish, and soy.There are different components that can trigger type 1 hypersensitivity responses, including antigens that come from: With this type of reaction, the body responds to an antigen by producing a specific type of antibody called IgE. Antigen/Antibody “Complexes” mainly deposit in the:–Kidney (Glomerular Basement Membrane)Ĭommon Type III Diseases:- Systemic Diseases:SLE, Polyarteritis nodosa, Post-streptococcal glomerulonephritis, Serum sickness (days).ġ.Type 1 hypersensitivity causes an immediate response and occurs after a person has exposure to an antigen.This phase is represented by fever, urticaria, arthralgias, lymph nodes enlargement and proteinuria. The third phase (acute inflammatory reaction): in this phase acute inflammatory reaction is initiated by activation of the complement cascade which in response activate neutrophils and monocytes.The second phase (Deposition of circulating complexes): In this phase the circulating complexes deposit in various tissues.The Abs react with the Ag in circulation and form Ag-Ab complexes. The first phase (formation of Ag-Ab complexes): In this Ag enters the body interacts with the immunocompetent cell which produces Abs against that Ag.In both of them the pathogenesis is divided into three phases: PATHOGENESIS (Mechanism) OF TYPE III (IMMUNE COMPLEX MEDIATED)HYPERSENSITIVITYType III hypersensitivity diseases may be systemic or local. Charge and three-dimensional structure of the immune complexes, the valency of the Ag, the affinity of the Ag to various tissue components and hemodynamic factors also play roles in the deposition of the complexes. It is the size of the complexes or the functional or structural abnormality of the mononuclear phagocytic cells which render the Ag-Ab complexes to be deposited in various locations. Ag-Ab complexes are formed in this disorder which deposits in various tissues and induce inflammation in them and gradually destroys them.Īg-Ab complexes formation is a normal phenomenon in most of the situations but they do not deposit normally.
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