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Immune System
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Skin Secretions Lysozyme Tears mucus, saliva Innate Defenses
External defenses Skin Secretions pH=3-5 Lysozyme Tears mucus, saliva
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Mucus Membranes
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Internal Innate Defense:
Phagocytosis Phagocytic cells Migrate OUT of the blood when the sense differences in concentration of certain chemicals engulf bacteria, dead cells, etc….
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Natural Killer Cells Recognize surface molecules on abnormal cells (cancerous or virus infected)
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Inflammatory response
Pin Skin surface Swelling Bacteria Phagocytes and fluid move into area Phagocytes Chemical signals White blood cell Blood vessel 1 Tissue injury; release of chemical signals such as histamine 2 Dilation and increased leakiness of local blood vessels; migration of phagocytes to the area 3 Phagocytes (macrophages and neutrophils) consume bacteria and cell debris; tissue heals link
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Pin Skin surface Bacteria
Fig. 24-2a Pin Skin surface Bacteria Chemical signals White blood cell Blood vessel 1 Tissue injury; release of chemical signals such as histamine
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Dilation and increased leakiness of local blood vessels; migration of
Fig. 24-2b Swelling Phagocytes and fluid move into area 2 Dilation and increased leakiness of local blood vessels; migration of phagocytes to the area
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Phagocytes (macrophages and neutrophils) consume
Fig. 24-2c Phagocytes 3 Phagocytes (macrophages and neutrophils) consume bacteria and cell debris; tissue heals
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Lymphatic system includes: -vessels (with valves) -fluid (lymph)
-organs Important cells involved are T lymphocytes and B lymphocytes These cells are responsible for specific immune responses to specific pathogens
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Acquired Immunity (the immune response)
Is highly specific Produces antibodies in response to specific antigens Antigens may be molecules on bacteria, viruses, protozoa, worms, transplanted organs Both B and T lymphocytes have receptors on membrane that recognize different antigens
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-do not produce antibodies -cytotoxic T cells
B cells -mature in bone - produce antibodies -antibodies float through the blood, recognizing and attaching to antigens T cells -mature in thymus -do not produce antibodies -cytotoxic T cells - require cell/cell contact to destroy pathogen Both B cells and T cells can produce memory cells
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Humoral immune response Cell-mediated immune response
Fig. 24-5a Humoral immune response Cell-mediated immune response Bone marrow Stem cell Thymus Via blood Immature lymphocytes Antigen receptor Antigen receptor B cell T cell Via blood Lymph nodes, spleen, and other lymphatic organs Final maturation of B and T cells in lymphatic organ
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Humoral immune response Cell-mediated immune response
Fig. 24-5a Humoral immune response Cell-mediated immune response Bone marrow Stem cell Thymus Via blood Immature lymphocytes Antigen receptor Antigen receptor B cell T cell Via blood Lymph nodes, spleen, and other lymphatic organs Final maturation of B and T cells in lymphatic organ
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Primary Immune Response
T cells are selected B cells are selected -antibody producing plasma cells are produced Person feels ill while these cells are produced Symptoms diminish as these cells do their job
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Secondary Immune Response
Response is much faster Memory cells are activated -tend to have a stronger response than the primary
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Primary immune response Antigen receptor (antibody on cell surface)
Fig. 24-7aa-1 Primary immune response 1 Antigen receptor (antibody on cell surface) B cells with different antigen receptors
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Primary immune response Antigen receptor (antibody on cell surface)
Fig. 24-7aa-2 Primary immune response 2 1 Antigen receptor (antibody on cell surface) Antigen molecules B cells with different antigen receptors
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Primary immune response Antigen receptor (antibody on cell surface)
Fig. 24-7aa-3 Primary immune response 2 1 Antigen receptor (antibody on cell surface) Antigen molecules B cells with different antigen receptors 3 First exposure to antigen Cell activation: growth, division, and differentiation
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Plasma (effector) cells secreting antibodies
Fig. 24-7aa-4 Primary immune response 2 1 Antigen receptor (antibody on cell surface) Antigen molecules B cells with different antigen receptors 3 First exposure to antigen Cell activation: growth, division, and differentiation Antibody molecules 4 Endoplasmic reticulum First clone Plasma (effector) cells secreting antibodies
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Plasma (effector) cells secreting antibodies Memory cells
Fig. 24-7aa-5 Primary immune response 2 1 Antigen receptor (antibody on cell surface) Antigen molecules B cells with different antigen receptors 3 First exposure to antigen Cell activation: growth, division, and differentiation Antibody molecules 4 5 Endoplasmic reticulum First clone Plasma (effector) cells secreting antibodies Memory cells
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Plasma (effector) cells secreting antibodies Memory cells
Fig. 24-7aa-6 Antigen molecules 6 Second exposure to same antigen Secondary immune response (May occur long after primary immune response.) Antibody molecules Endoplasmic reticulum Second clone Plasma (effector) cells secreting antibodies Memory cells
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Fig T cells work by directly binding to infected cells and then destroying them 1 Cytotoxic T cell binds to infected cell Self-nonself complex Foreign antigen Infected cell Perforin molecule Cytotoxic T cell
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Perforin makes holes in infected cell’s membrane and enzyme enters
Fig 1 Cytotoxic T cell binds to infected cell 2 Perforin makes holes in infected cell’s membrane and enzyme enters Self-nonself complex Hole forming Foreign antigen Infected cell Perforin molecule Cytotoxic T cell
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Perforin makes holes in infected cell’s membrane and enzyme enters
Fig 1 Cytotoxic T cell binds to infected cell 2 Perforin makes holes in infected cell’s membrane and enzyme enters 3 Infected cell is destroyed Self-nonself complex Hole forming Foreign antigen Infected cell Perforin molecule Cytotoxic T cell
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Allergies Hypersensitivity to environmental antigen (allergen)
Antibodies attach to mast cells - later, allergen attaches to these antibodies on mast cells Histamine & other inflammatory agents released
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Antigenic determinant Histamine
Fig a B cell (plasma cell) Mast cell Antigenic determinant Histamine 1 Allergen (pollen grain) enters bloodstream 2 B cells make antibodies 3 Antibodies attach to mast cell Sensitization: Initial exposure to allergen
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Later exposure to same allergen
Fig b 4 Allergen binds to antibodies on mast cell 5 Histamine is released, causing allergy symptoms Later exposure to same allergen
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Anaphylactic shock Acute reaction to allergen
Massive dilation of blood vessels -drop in blood pressure Counteracted by epinephrine
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Active immunity Passive immunity
results from natural recovery from infections vaccinations Passive immunity Receive antibodies from someone else -IgG anitibodies cross placenta -breast milk -shots (rabies treatment)
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Transfusions/transplants
ABO blood group -IgM doesn’t cross placenta Antibodies produced against bacterial antigens which are very similar rH factor -IgG crosses placenta
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Tissue graphs/ organ transplants
Give drugs that suppress cell mediated immunity Bone marrow transplants Risk of graft vs host reaction Donor lymphocytes attack host cells
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Autoimmune diseases Immune system doesn’t recognize “self” and attacks
MS Insulin dependent diabetes
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AIDS HIV infection of cells require CD4 -found on T cells
Is a retrovirus Antibodies are ineffective because -provirus gives it “invisibility” -rapid rate of mutation -Helper T cells decrease -secondary infections Drug treatments slow viral replication -AZT (reverse transcriptase inhibitors) -protease inhibitors
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