Immune System
pH=3-5•Skin•Secretions •Lysozyme
•Tears•mucus,•saliva
Mucus Membranes
Phagocytic cells
Migrate OUT of the blood when the sense differences in concentration of certain chemicals engulf bacteria, dead cells, etc….
Recognize surface molecules on abnormal cells (cancerous or virus infected)
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
Fig. 24-2a
Pin
1
Skin surface
BacteriaChemicalsignals
Whiteblood cell
Blood vessel
Tissue injury; release ofchemical signals such ashistamine
Fig. 24-2b
2
Swelling
Phagocytes andfluid moveinto area
Dilation and increasedleakiness of local bloodvessels; migration ofphagocytes to the area
Fig. 24-2c
3
Phagocytes
Phagocytes (macrophagesand neutrophils) consumebacteria and cell debris;tissue heals
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
•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)
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
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
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
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
Response is much faster
Memory cells are activated -tend to have a stronger response than the primary
Fig. 24-7aa-1
Primary immuneresponse
B cells withdifferentantigenreceptors
Antigen receptor(antibody on cellsurface)
1
Fig. 24-7aa-2
Primary immuneresponse
B cells withdifferentantigenreceptors
Antigen receptor(antibody on cellsurface)
1 Antigenmolecules
2
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
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
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
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.)
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
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
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
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
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
Fig. 24-17b
Allergen binds toantibodies onmast cell
Histamine isreleased, causingallergy symptoms
Later exposure to same allergen
4 5
Anaphylactic shock
Acute reaction to allergen
Massive dilation of blood vessels-drop in blood pressure
Counteracted by epinephrine
Active immunityresults from natural recovery from infections
vaccinations
Passive immunityReceive antibodies from someone else
-IgG anitibodies cross placenta-breast milk-shots (rabies treatment)
Transfusions/transplantsABO blood group
-IgM doesn’t cross placenta
Antibodies produced against bacterial antigens which are very similar
rH factor-IgG crosses placenta
Tissue graphs/ organ transplants
Give drugs that suppress cell mediated immunity
Bone marrow transplants
Risk of graft vs host reactionDonor lymphocytes attack host cells
Autoimmune diseasesImmune system doesn’t recognize “self” and attacks
MS
Insulin dependent diabetes
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
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