immune system. ph=3-5 skin secretions lysozyme tears mucus, saliva
TRANSCRIPT
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Immune System
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pH=3-5•Skin•Secretions •Lysozyme
•Tears•mucus,•saliva
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Mucus Membranes
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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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Recognize surface molecules on abnormal cells (cancerous or virus infected)
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Pin
1 2 3
SwellingSkin surface
Bacteria
Chemicalsignals
Whiteblood cell
Blood vessel
Phagocytes andfluid moveinto area
Phagocytes
Tissue injury; release ofchemical signals such ashistamine
Dilation and increasedleakiness of local bloodvessels; migration ofphagocytes to the area
Phagocytes(macrophages andneutrophils) consumebacteria and celldebris; tissue heals
link
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Fig. 24-2a
Pin
1
Skin surface
BacteriaChemicalsignals
Whiteblood cell
Blood vessel
Tissue injury; release ofchemical signals such ashistamine
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Fig. 24-2b
2
Swelling
Phagocytes andfluid moveinto area
Dilation and increasedleakiness of local bloodvessels; migration ofphagocytes to the area
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Fig. 24-2c
3
Phagocytes
Phagocytes (macrophagesand neutrophils) consumebacteria 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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•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
Acquired Immunity (the immune response)
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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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Fig. 24-5a
Humoral immuneresponse
Cell-mediatedimmune response
Lymph nodes,spleen, and
other lymphaticorgans
Final maturationof B and T cells inlymphatic organ
Viablood
T cellB cell
Viablood
Antigenreceptor
Thymus
Antigenreceptor
Immaturelymphocytes
Stem cell
Bonemarrow
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Fig. 24-5a
Humoral immuneresponse
Cell-mediatedimmune response
Lymph nodes,spleen, and
other lymphaticorgans
Final maturationof B and T cells inlymphatic organ
Viablood
T cellB cell
Viablood
Antigenreceptor
Thymus
Antigenreceptor
Immaturelymphocytes
Stem cell
Bonemarrow
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T cells are selected
B cells are selected-antibody producing plasma cells are produced
Person feels ill while these cells are producedSymptoms diminish as these cells do their job
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Response is much faster
Memory cells are activated -tend to have a stronger response than the primary
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Fig. 24-7aa-1
Primary immuneresponse
B cells withdifferentantigenreceptors
Antigen receptor(antibody on cellsurface)
1
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Fig. 24-7aa-2
Primary immuneresponse
B cells withdifferentantigenreceptors
Antigen receptor(antibody on cellsurface)
1 Antigenmolecules
2
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Fig. 24-7aa-3
Primary immuneresponse
B cells withdifferentantigenreceptors
Antigen receptor(antibody on cellsurface)
1 Antigenmolecules
2
First exposureto antigen
Cell activation:growth,division, anddifferentiation
3
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Fig. 24-7aa-4
Primary immuneresponse
B cells withdifferentantigenreceptors
Antigen receptor(antibody on cellsurface)
1 Antigenmolecules
2
First exposureto antigen
Cell activation:growth,division, anddifferentiation
3
Antibodymolecules
EndoplasmicreticulumFirst clone
Plasma (effector) cells secreting antibodies
4
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Fig. 24-7aa-5
Primary immuneresponse
B cells withdifferentantigenreceptors
Antigen receptor(antibody on cellsurface)
1 Antigenmolecules
2
First exposureto antigen
Cell activation:growth,division, anddifferentiation
3
Antibodymolecules
EndoplasmicreticulumFirst clone
Plasma (effector) cells secreting antibodies
4
Memory cells
5
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Fig. 24-7aa-6
Second clone
Plasma (effector) cells secreting antibodies Memory cells
6
Antigenmolecules
Second exposureto same antigen
Endoplasmicreticulum
Antibodymolecules
Secondaryimmuneresponse (Mayoccur long afterprimary immuneresponse.)
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Fig. 24-12-1
1 Cytotoxic T cell bindsto infected cell
Self-nonselfcomplex
CytotoxicT cell
Foreignantigen
Perforinmolecule
Infected cell
T cells work by directly binding to infected cells and then destroying them
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Fig. 24-12-2
1 Cytotoxic T cell bindsto infected cell
Self-nonselfcomplex
CytotoxicT cell
Foreignantigen
Perforinmolecule
Infected cell
Perforin makes holes ininfected cell’s membraneand enzyme enters
Holeforming
2
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Fig. 24-12-3
1 Cytotoxic T cell bindsto infected cell
Self-nonselfcomplex
CytotoxicT cell
Foreignantigen
Perforinmolecule
Infected cell
Perforin makes holes ininfected cell’s membraneand enzyme enters
Holeforming
2 Infected cellis destroyed
3
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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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Fig. 24-17a
B cell(plasma cell)
Mastcell
HistamineAntibodiesattach tomast cell
Antigenic determinant
B cells makeantibodies
Allergen (pollen grain)enters bloodstream
Sensitization: Initial exposure to allergen
1 2 3
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Fig. 24-17b
Allergen binds toantibodies onmast cell
Histamine isreleased, causingallergy symptoms
Later exposure to same allergen
4 5
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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 immunityresults from natural recovery from infections
vaccinations
Passive immunityReceive antibodies from someone else
-IgG anitibodies cross placenta-breast milk-shots (rabies treatment)
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Transfusions/transplantsABO 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 reactionDonor lymphocytes attack host cells
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Autoimmune diseasesImmune system doesn’t recognize “self” and attacks
MS
Insulin dependent diabetes
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HIV infection of cells require CD4-found on T cells
Is a retrovirusAntibodies 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