Infection and Immunity - 5

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  • Created by: LBCW0502
  • Created on: 22-11-19 10:34
Where do antibodies come from? (1)
Antibodies are not made all the time. Large amounts not produced due to tolerance and metabolic cost. Antibodies produced by B cells (large nucleated cells)
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Where do antibodies come from? (2)
Bone marrow stem cells, B cells, contact with antigen, B cell differentiates into either plasma cell (produce antibodies) or memory cell (for secondary response). B for 'bursa' (study in chicken)
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Describe features of the clonal selection model (1)
Antigen specific to Ab receptor, contact between antigen and antibody, B cell will rapidly divide/differentiate into plasma or memory cells (clonal selection/expansion)
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Describe features of the clonal selection model (2)
Produce specific antibody (can produce different classes of antibody e.g. IgG, IgM but specificity remains the same)
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How to antigens trigger B-cells to make antibodies? (1)
B cells need receptor on surface to recognise antigen (BCR - B-cell presents on its surface the antibody which it produces). Antibody binding site will have specificity for a given antigen
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How to antigens trigger B-cells to make antibodies? (2)
Bind to F ab regions. Depends on complexity on antigen (complex antigen - can cross-link BCRs, one BCR may not trigger antibodies)
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What are thymus independent antigens?
Trigger B cell to produce antibody, critical matrix formed. In a less complicated antigen - can still have sufficient cross linking of BCRs (non-specific activation) - turn on B cells to produce antibodies
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Can all antigens turn B cells on?
Not all antigens can turn on a B cell (thymus dependent)
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Describe features of T cells (1)
Help B cells produce antibodies (T helper cells), come from haematopoetic stem cells in bone marrow, processed in the thymus (large organ as a baby due to immune system development, processed T cells as adults, thymus disintegrates)
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Describe features of T cells (2)
Immature T cells in secondary lymphoid tissue, differentiates when they come into contact with antigens
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What are the two types of T helper cells?
Th1 and Th2
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Which of the T helper cells helps B cells produce antibodies?
Th2 cells
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Describe functions of T helper cells (1)
Phagocytosis of bacteria. Phagolysosome formed. Degradation to give individual peptides, MHC II molecules formed, form a complex with cell debris, expression on surface of APC (macrophage). Macrophage expresses MHC II and debris from digested bacteri
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Describe functions of T helper cells (2)
TCR only specific for certain antigen. T cell and B cell both have specificity. (Lock and key model). CD4 cells (Th2 cells - aid stabilisation of TCR binding to MCH II and peptide complex)
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Describe functions of T helper cells (3)
Results in generation of cytokines (IL 2/4/5 - turn on B cell to produce antibody)
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How is the function of T helper cells amplified? (1)
Few T cells in lymphatic system (need to amplify this using macrophages) - macrophage already in contact with bacterium (phagocytosis). T helper cell can recognise antigen (with MHC II) with TCR. Bind to macrophage
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How is the function of T helper cells amplified? (2)
IL-1 formed (clonal expansion of T cell, more likely for B cell to come into contact with T cell to produce antibodies, amplification)
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How is the function of T helper cells amplified? (3)
If macrophage presents antigen, able to over produce macrophages (amplification). Th1 cells help macrophages, Th2 cells help B cells
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How is the function of T helper cells amplified? (4)
Macrophage takes up bacteria via phagocytosis, express antigen on surface with MHC II. Th 1 cell with TCR joints to MHC II/antigen complex, produce cytokines, increase phagocytosis. Inducer T cells, delayed type hypersensitivity cells
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Describe the use of T cells to respond to virally infected cells (1)
Th1 cell can interact with cytotoxic T cell - turn on killer T cell, attack virally infected cell. Cell will process viral proteins with MHC I onto surface, T cell with TCR binds to complex, stabilised by CD8 (Th1)
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Describe the use of T cells to respond to virally infected cells (2)
Stimulate cytotoxic cells to degranulate. Cytotoxic T cells also called CD8 cells
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Describe features of the adaptive cell mediated immunity to virally infected cells (1)
Virally infected cell starts to produce interferon alpha/beta (protects uninfected cells), infected cells stop expressing MHC I molecules (non-self), activate NK cells. Some infected cells express MHC I (binds to cytotoxic T/CD8 cell, destroy cell)
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Describe features of the adaptive cell mediated immunity to virally infected cells (2)
Some infected cells express MHC II (bind to T cell/CD4, macrophage activation and NK cell activation). Effector T cells also known as cytotoxic T cells
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Summarise the five features of the adaptive immunity
(Recognition, specificity of non-self). B-cells. Th2 T cells, Th1 T cells. Effector T cells (cytotoxic T cells). Receptors and cytokines
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What happens when regulation of the immune response fails?
Can result in hypersensitivity (allergy) - abnormal response via immune system (manifestation of immune response) e.g. rhinitis, touch allergy, nut allergy (inflammatory response - can be fatal)
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What is type I hypersensitivity? (1)
Anaphylactic sensitivity. IgE causes mast cell degranulation. Antibody - Fc region, complement classical pathway or bind antigen to macrophage, mast cell involved. IgE binds to mast cell, cross-linking between IgE molecules (critical matrix)
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What is type I hypersensitivity? (2)
Certain allergens can cause cross-linking to occur, leading to premature mast cell degranulation. E.g. bee sting, stinging nettles, nut allergy, penicillin
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What is type II hypersensitivity? (1)
Antibody dependent cytotoxic hypersensitivity. Introduce antigen into the body, body responds with antibody e.g. blood transfusion, transplantation, antibody dependent
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What is type II hypersensitivity? (2)
Introduce blood into recipient, recipient has different blood type to donor (expresses different antigens on rbc compared to the donor, recognised as non-self), immune system produces antibodies against rbc, activate complement pathway/phagocytosis
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What is type III hypersensitivity?
Complex mediated hypersensitivity. Ag-Ab complexes remain for a long period of time (not broken down), can cause platelet aggregation, cause complement activation, cause anaphylactic shock, occurs around joints
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What is type IV hypersensitivity? (1)
Cell mediated or delayed type hypersensitivity. Macrophage (phagocytosis of bacteria), expression on surface, stimulation T cell, cause clonal expansion of Th2 cell, cause lymphokines to be produced, super antigens
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What is type IV hypersensitivity? (2)
T cells produce lots of lymphokines, over-reaction of macrophage (giant cells), joint together to form granulomas (Th1 - overproduction of cytokines, over-reaction and T killer cells, cytotoxicity, cause tissue damage)
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Other cards in this set

Card 2

Front

Where do antibodies come from? (2)

Back

Bone marrow stem cells, B cells, contact with antigen, B cell differentiates into either plasma cell (produce antibodies) or memory cell (for secondary response). B for 'bursa' (study in chicken)

Card 3

Front

Describe features of the clonal selection model (1)

Back

Preview of the front of card 3

Card 4

Front

Describe features of the clonal selection model (2)

Back

Preview of the front of card 4

Card 5

Front

How to antigens trigger B-cells to make antibodies? (1)

Back

Preview of the front of card 5
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