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57 Cards in this Set
- Front
- Back
innate immunity
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defense against any pathogen
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adaptive immunity
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induced resistance to a specific pathogen
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humoral immunity
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b-cell mature in rbm
due to antibodies from bcell |
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cellular immunity
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due to t- cells
t-cell mature in the thymus |
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antigen
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causes body to produce specific antibodies or sensitized t-cell
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immunoglobulins
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globular proteins
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valence
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determines by the number of antigen-binding sites
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serology
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he study of reaction between antibodies and antigens
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antiserum
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the generic term for serum that contains Ab
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cytokine
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chemical messanger
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cytokine storm
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over production of cytokine
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globulins
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serum proteins
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immunoglobulins
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antibodies
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gamma globulins
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serum fraction contain Ab
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MHC-major histocompatibility complex
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distinguishes self from non cells
"password" |
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T-dependent antigens
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need MHC to make t-helper cells
t helper cells produce cytokine that activates bcells |
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t-independent antigens
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stimulate bcells to make Abs
doesnt need MHC |
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clonal deletion
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eliminates harmful bcells
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Th1
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produces gamma IFN that activate cell related to cell mediated immunity like macrophages and Ab
-useful against viruses |
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Th2
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activates eosinophil and bcells to produce Igt
-useful aganist bacteria and parasites |
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what nature does adaptive immunity have
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dual
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3 steps to dual adaptive immunity
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1. stem cells develop from stem cells in rbm
2. 2 cell lines formed: bcells in rbc and tcells in thymus |
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2 adaptive immunities
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1. humoral
2. cellular |
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2 things antibodies interact with
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1. epitopes-recognized by antibodies
2. antigenic determinants -part of RNA/DNA |
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7 properties of IgG antibodies
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1. monomer
2. 80% of serum is antibodies 3. fix complement 4. in blood, lymph, and intestines 5, cross placenta 6. enhances phagocytosis, neutralizes toxins and viruses protect fetus, new born 7. half life is 23days |
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6 IgM antibody properties
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1. pentamer
2. 5-10% serum is antibodies 3. fit compement 4. in blood, lymph, on bcells 5. agglutinates microbes, first Ab produced in response to infection 6. half life is 5 days |
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5 IgA antibody properties
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1. dimer
2. 10-15% serum is antibodies 3. in secretions 4. mucosal protection 5. half life is 6 days |
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5 IgD properties
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1. monomer
2. 0.02% serum is antibodies 3. in blood, lymphs, on bcells 4. on bcells initiated immune response 5. 1/2 life 3 days |
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5 IgE properties
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1. monomer
2. 0.002% of serum in Ab 3. on mast cell, basophils, and in blood 4. allergic reactions, lysis, parasitic worms 5. 1/2 life 2 days |
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5 parts to clonal selection
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1. stem cells differentiate into mature bcells with immunoglobulins against specific antigen
2. bcell 3 complexs with its specific antigen and proliferate 3. some bcells proliferate intolong lived memeroy cells which later can be antibody producers 4. other bcells proliferate into antibody producing plasmacells 5. plasma cells secrete antibodies into circulation |
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bcells differentiate into
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1. antibody producing plasma cells
2. memory cells |
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aggulation
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reduces the number of infectious unit to deal with
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activation of complement
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causes inflammation and cell lysis
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opsonization
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coating antigens with antibodies enhancing phagocytosis
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antibody cell mediated cytotoxicity
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antibodies attached to target cell cause destruction by macrophages eosinophils and NK cells
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neutralization
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blocks adhesion of bacteria and viruses to mucosa
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5 protective mechanisms of binding antibodies
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1. aggulation
2. activated complement 3. opsonization 4. antibody dependent cell mediated cytotoxicity 5. neutralization |
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4 properties of tcell
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1. mature in thymus
2. respond to Ag to TCR 3. require APC 4. pathogens enter gastrointestinal and respiratory tracts thro mcells over peyers patch which has APC |
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thymic selection
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eliminates immature t-cel e
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2 forms of t-helper cells
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Th1
Th2 |
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4 properties of t cytotoxicity cells
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1. celled: CD8+ or Tc cells
2. target cells are self carrying endogenous antigens 3. activated into CTL cytotoxic gamma lymphocytes -CTL recognizes ag and MHC -induces apoptosis in target cells 4. CTL releases perforin and granzymes |
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3 steps to t-cytotoxic cell performance
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1. virus infected cells or cancer cells prduce abnormal endrogenous antigens
2. abnormal antigens are presented on the cell surface in association with MHC class one molecules -CD8 receptors transform into CTL 3. CTL induces destruction of viruses infected by apoptosis |
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antigen presenting cell
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digest antogens
have Ag fragments on APC surface that interact with MHC -bcell -dendritic cells -activated macrophages |
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3 functions of NKC
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1. glandular leukocytes destroy cells that dont express MHC
2. kill viruses infected and tumor cells 3. attack parasites |
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8 cytokine
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1. interleukin 1
2. IL-2 3. IL-3 4. IL-4/5 5. chemokines 6. hemotooletic cytokines 7. IFN alpha and beta 8. IFN gamma |
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IL-1
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stimulate T-helper cells in presence of antigens
attrats phagocytes |
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IL-2
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proliferation of antigen-stimulates Cd4+thC
proliferation and differentiation of bcells activation of CD8 and NKC |
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chemokins
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induce the migration of leukocytes
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TNF alpha
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promotes inflammation
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hematopoietic cytokine
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influence differentiation of blood stem cells
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IFN alpha/beta
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responds to viral infection
interferes with protein synthesis |
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IFN gamma
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stimulates macrophage activity
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3 steps to immunological memory
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antibody titer
primary response secondary response |
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antibody titer
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amount of Ab in serum
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primary response
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occurs after initial contact with Ag
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secondary response
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occurs after second exposure
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4 types of adaptive immunity
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1. naturally acquired active
2. naturally acquired passive 3. artificially acquired active 4. artificially acquired passive |