Unit 1: Hypersensitivity and Autoimmunity
About this set
Created by:
jem19047 Plus on October 12, 2011
Subjects:
Log in to favorite or report as inappropriate.
Order by
62 terms
Terms | Definitions |
|---|---|
 hypersensitivity | is the exaggeration of normal immune response to foreign substances |
| hypersensitivity | incidental tissue damage- due to out of control immune response caused by a ... |
| type 1 | ... hypersensitivity is immediate, and is the classic "allergic reaction" to food and insect bites as well as asthma |
| allergic reaction | type 1 immediate hypersensitivty is the classic ... to food and insect bites as well as asthma |
| IgE | .... secreted by plasma cells is bound to the outside of mast cells and basophils via interaction of the Fc portion |
| bridging | ... occurs in the type 1 immediate hypersensitivity immune reaciton in which when two nearby IgE molecules are bound, signals mast cells to release inflammatory mediators |
| C3a and C5a | in the type 1 immediate hypersensitivity immune reaction, complement proteins... can do the same thing that bridged IgE's can do, and stimulate mast cells to release their inflammatory mediators |
| mediators | in the type 1 immediate hyersensitivity immune reaction, the preformed ... in the mast cells and other granular cells includes histamine, chemokines, lysosomal enzymes, heparin |
| histamine, chemokines, lysosomal enzymes, heparin | are the preformed mediators found in granular cells such as mast cells that work in the inflammatory process of type 1 hypersensitivty |
| histamine | ... is one of the preformed mediators found in mast cells involved in type 1 hypersensitivity immune response, and increases the permeability of blood capilaries to other immune cells |
| chemokines | ... are one of the preformed mediators found in the mast cells invovled in the type 1 hyerpsentivity response that induces chemotaxis of other immune cells (eosinophils and neutrophils) to its location |
| lysosomal enzymes | ... are some of the preformed inflammatory mediators found in mast cells that are a part of the type 1 hypersensitivity immune reaction that help to destroy harmful particles in environment by lysing them |
| heparin | ... is another preformed inflammatory mediator found in mast cells invovled in the type 1 hypersensitivity immune response that is an anticoagulant agent that keeps blood moving in that area |
| allergic reaction | in the classic ... of type 1 hypersensitivity we see a clincial presentation of hives (urticaria), itching (pruritis), edema, diarrhea |
| anaphylaxis | in the ... type 1 hypersensitivity reaction we see a clinical presentation of hypotension, bronchoconstriction |
| mast | once ... cells degranulate in the type 1 hypersensitivty reaction, in ... cell will see an increased synthesis of prostaglandins and leukotrienes which can lead to a lasting type 1 hypersensitivity response (asthma) |
| asthma | ... is the lasting type 1 hypersensitivity caused by the secretion of prostaglandins and leukotrienes by degranulated mast cells |
| prostaglandins and leukotrienes | ... are the 2 chemical secreted after degranulation of a mast cell in type 1 hypersensitivity reaction, which gives us a lasting immune response (such as asthma) |
| drugs or metabolites | Classically, .... stick to the cell membrane of normal cells |
| foreign | Normal cell proteins plus hapten yields an immunologically "...." substance |
| type 2 | ... hypersensitivity is called cell-bound hypersensitivity |
| Antibodies | .... bound to cell can trigger complement cascade, enhance phagocytosis and promote local tissue damage by neutrophils, causing a type 2 hypersensitivity reaction |
| cell-bound, type 2 | Classic example of a .... hypersensitivity is drug-induced hemolytic anemia, thrombocytopenia, or leukopenia |
| autoantibodies | type 2 cell-bound Antibodies created in response to hapten bound to host cell can also be ..... to normal cellular proteins, which can lead to autoimmune disease |
| Pemphigus | ... is an example of a type 2 cell-bound hypersensitivity in which host makes antibody to fight infection that is similar to host cell's dermal joint proteins (so body will attack normal dermal joint protein--> blisters all over) |
| Goodpastures | ... is another example of a type 2 cell-bound hypersensitivity in which host makes an antibody that is also an autoantibody to glomerular and respiratory basement membrane proteins (causes kidney and respiratory problems) |
| immune complex | ... aka type 3 hypersensitivity is caused by deposition of circulating antibody-antigen complexes, and these deposited complexes can activate complement |
| type 3, immune complex | .... hypersensitivity is historically seen as "serum sickness" when people received repeated infusions of animal serum to neutralize toxic products (i.e. tetanus) |
| type 3, immune complex | ... hypersensitivity is now mostly seen in cases where bacterial antigen-antibody complexes lodge in renal basement membrane (in post-streptococcal glomerulonephritis) and in lupus |
| delayed, type 4 | ... hypersensitivity is the cause of many skin reactions such as tuberculin reaction (PPD) and contact dermatitis (poison ivy or poison oak), due to T cell-mediation |
| delayed, type 4 | the .... hypersensitivity occurs when T-cells in the skin have been previously exposed to an antigen, and upon repeat exposure, a robust, but delayed reactions occurs and includes induration: edema and fibrin deposition in that area |
| delayed, type 4 | the .. hypersensitivity Involves recruitment of more lymphocytes and macrophages, but is a typically limited course, assuming antigen exposure is only temporary |
| delayed, type 4 | the ... hypersensitivity classic example is the PPD test. Takes T cells longer to cause reaction than antibodies. If one exposure- T cells that have receptor that matches foreign product then they are stimulated. So next time T cells have been primed and act more quickly but takes 24 to 48 hours. SO see edema and fibrin deposit at site of injection |
| delayed, type 4 | if the ... hypersensitivity reaction is chronic due to chronic exposure to antigen, can lead to formulation of granulomas at site if irriation |
| Autoimmunity | ... is Immune response to antigens which should not illicit an immune response, so self does not recognize self--> breakdown in recognition |
| autoimmunity | ... is the Breakdown in the normal process of self-tolerance |
| autoimmunity | ... is "Tricking" the immune system into attacking self antigens |
| T cells | immature T cells go to thymus to be educated and there they are where negatively selected based upon too strong a response to self antigens, so this helps to prevent autoimmune disease |
| antigen presenting cells | Many antigens are sequestered from entering the blood/lymph and so can not travel to lymph nodes and be taken up by .....s there which helps to reduce risk of autoimmune disease |
| B cell | even if you have a self reacting ... the T cell education in thymus should eliminate its helper T cells which need to provide costimulation for maturation and production of antibodies from this lymphocyte (helps to limit autoimmune disease) |
| antigen presenting cells | some T cells in healthy tissue might recognize self antigens, but local ... do not recognize these antigens, so they will not be activated and will not provide the necessary costimulation causing the T cell to under go anergy (helps to prvent autoimmune disease) |
| suppressor T-cells | Small subset of .... which can secrete anti-inflammatory cytokines if they see self- turn off response of other autoimmune processes that may be occuring |
| tolerance | breakdown of ... of self occurs when When tissue damage occurs (trauma or inflammation) antigens previously sequestered may enter circulation |
| proteolytic | breakdown of tolerance of self can also occur when Local inflammation may increase .... activity which exposes/creates new antigens from self proteins |
| costimulatory | breakdown of tolerance for self can also occur when APCs in tissue which is already inflamed may be induced to express ... molecules |
| Suppressor T-cells | breakdown of tolerance of self can also occur when .... may be downregulated by other activated inflammatory cells |
| tolerance | Once ... of self breaks down it is relatively easy for it to become self-sustaining (epitope spreading) |
| molecular mimicry | ... is another way that breakdown of self tolerance can occur and happens when proteins from various bacteria and viruses may bear some resemblance to self antigens, and when an immune response is mounted against these microbial proteins, there is a small amount of cross-reactivity |
| genetics | ... undoubtedly plays a role in some autoimmune diseases with HLA type being the classic example HLA B27 : ankylosing spondylitits- problem with spine, Reiter's syndrome DR2 :Goodpasture's syndrome DR3 : Hashimoto's thyroiditis- oposite of graves- antibody binds and turns off thyroid, myasthenia gravis DR4 :Type I diabetes |
| HLA | ... type (molecule presented to B and T cells) is the classic example of a genetic cause of autoimmune disease |
| Environmental | .... factors are even more likely to contribute to autoimmunity |
| females | Most autoimmune diseases are more prevalent in ... (estrogen) |
| molecular mimicry | Infection creates a pro-inflammatory state and can cause autoimmunity due to ... but at the same time conditions which are too aseptic promote autoimmune disease |
| drugs | Certain ... can act as haptens with self antigens |
| UV | .. radiation can alter (skin) self antigens and/or increase expression of some proteins |
| Systemic Lupus Erythematous | ... is a systemic autoimmune disorder which can affect almost any organ, and is basically, a Type III hypersensitivity reaction to self antigens. Special predilection for skin, kidney, serosal surfaces, joints and heart Onset typically in adolescence or early adulthood Women and AA are especially at risk, 1:245 for AA women of child bearing age |
| Systemic Lupus Erythematous | the exact cause of ... is unknown but there is a breakdown of both T-cell and B-cell tolerance |
| genetic | there is a ... component to systemic lupus erythematous 50% concordance in monozygotic twins 20% of family members who are clinically silent have detectable autoantibodies |
| environmental | there is also an ... component to systemic lupus erythematous, and this has been seen in : UV exposure increases severity of skin lesions Drugs (procainamide, hydralazine) can induce lupus symptoms which eventually cease when drug is stopped |
| systemic lupis erythematous | in .... A variety of autoantibodies can be formed, but all are collectively called antinuclear antibodies DNA Histones Other proteins bound to nucleic acids Nucleolar antigens |
| antinuclear antibodies | ... are the major type of autoantibodies produced by a systemic lupis erythematous disease |
| Systemic Sclerosis | is an autoimmune disease in which we see Excess deposition of collagen in skin and organs (GI tract, joints, lungs, kidneys, heart) "Typical" patient is a 50-60 y/o female |
First Time Here?
Welcome to Quizlet, a fun, free place to study. Try these flashcards, find others to study, or make your own.