1. Immunity
Innate & Adaptive

2. Immunity Innate: response to attack is always the same
Mechanical mechanisms
Chemical mediators
Cellular response
Inflammatory response
Adaptive: response to attack improves with each exposure
Specific
Has memory

3. Innate immunity Mechanical mechanisms
Skin & mucus membranes form physical barriers to prevent entry
Tears, saliva, urine wash away pathogens from surface or body or dilute invading army of pathogens

4. Innate immunity
Chemical mediators: Some prevent entry to cells, kill bacteria, or produce inflammation
Complement proteins
~ 20 in plasma
normally inactive; activated by combining with parts of bacterial cells or antibodies
Leads to chain rxn activation of neighboring compliments & inflammation, phagocytosis, or lysis

5. Innate immunity Chemical mediators
Interferons protect against viral infection
Virus-infected cells place interferons on their surface (SOS signal)
These bind to neighboring cells & stimulate neighbors to produce antiviral proteins
Intiviral proteins inhibit production of new viral RNA
Some interferons activate macrophages and NKC

6. Innate immunity Cellular mechanisms
WBC & derivatives are most important cellular components
Attracted to invading bacteria and microorganisms through chemotaxis
Phagocytic cells (who are these?)
Inflammatory cells (…and these?)
Natural Killer Cells (NKC)

7. White Blood Cells

8. Innate immunity Phagocytic cells Neutrophils Macrophages
Small; first to enter infected tissue from blood; ingest, then die --> pus accumulation
Macrophages
Monocytes leave blood & enlarge; arrive after neutrophils; do most eating & cleanup
Also hang out at “entry points” (gate-keepers)

9. Innate immunity Natural Killer Cells (NKC)
15% of all lymphocytes are NKC
Recognize tumor cells or virus-infected cells (generalist killers)
No memory; non-specific
Kill via chemical release (cell membrane lysis)

10. Innate immunity
Inflammatory cells: activated through innate or adaptive immunity; release histamine & pyrogens
Basophils
Motile WBC; enter infected tissue
Mast cells
Non-motile; Located in lymph organs at “points of entry”
Eosinophils
Release enzymes that reduce inflammation (control)

11. Inflammation is useful!
Local inflammation: Redness, heat, swelling
caused by increased blood flow & vascular permeability
Chemicals and swelling activate pain receptors
Systemic inflammation
Red marrow increases neutrophil production
Pyrogens stimulate fever by increasing heat production & conservation
Vascular permeability increases

12. Adaptive immunity Lymphocytes Antibody-mediated Cell-mediated
Origin & development
Activation & multiplication
Antibody-mediated
Cell-mediated

13. Adaptive immunity Antigens stimulate adaptive immune response
Self
Foreign
MHC molecules display antigens
Lymphocytes
Origin & development
Activation & multiplication
Types of Adaptive Immunity
Antibody-mediated
B cells; produce cells that make antibodies
Cell-mediated
T cells; cytotoxic & helper T cells

14. Antigens
Foreign
Components of bacteria, viruses, and their chemical byproducts
Pollen, animal hair, foods produce allergic response (overreaction of immune system)
Self
Produced by our bodies
Recognize tumor antigens

15. B & T-cells (Lymphocytes)
Contain antigen receptors in their cell membranes
We each have thousands of different populations of B & T-cells, each with unique antigen receptors
Cells are stimulated by binding of antigens to their unique receptors

16. Cell Development Red marrow produces:
Lymph nodes,
spleen, and
other lymphatic
organs
Final maturation
of B and T cells in
lymphatic organ
Via
blood
T cell
B cell
Antigen
receptor
Thymus
Immature
lymphocytes
Stem cell
Bone
marrow
Cell Development
Red marrow produces:
Pre B-cells: released into bloodstream
migrate to lymph organs
Pre T-cells: migrate to thymus & mature there
Mature T-cells migrate to lymph organs

17. Activation & multiplication
Macrophages present antigens
Phagocytize invaders, process & display antigens (with help of MHC molecules)
MHC/Antigen complex binds to receptors on B or T-cells
T-cells auto-stimulate
Produce cytokines (peptides; e.g. interleukin) that up-regulate growth & division

18. B cell activation Antibody-mediated
B-cells can also phagocytize & process antigens
same antigen that stimulated a Th
Th binds to B-cell
Interleukins are produced
stimulate B-cell division & proliferation
Daughter (plasma) cells produce antibodies

19. Effects of Antibodies Direct Indirect
Antibodies bind antigens = inactivation
Indirect
Activate Complement cascade
Inflammation (mast cells and basophils release histamine)
Chemotaxis (attracts white blood cells)
Phagocytosis or lysis (macrophage eats antibody & antigen

20. Binding of antibodies to antigens inactivates antigens by
Neutralization
Agglutination
of microbes
Precipitation of
dissolved antigens
Phagocytosis
Cell lysis
Activation of
complement system
Leads to
Foreign cell
Hole
Complement
molecule
Bacteria
Antigen
molecules
Enhances
Bacterium
Virus
Macrophage

21. Antibody production
Differs following first and second exposure to antigen
First exposure = primary response
B-cells bind antigen; produce plasma cells (produce antibodies) and memory B-cells
Response time = 3-14 days; disease symptoms develop; SLOW

22. 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

23. 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

24. 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

25. 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

26. 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

27. Antibody production
Differs following first and second exposure to antigen
Second exposure = secondary response
Memory cells quickly induce plasma cells to produce antibodies
Time to antibody production is reduced
More plasma cells & antibodies produced
RAPID response, no disease symptoms = immunity

28. 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

29. Secondary immune response to antigen X Primary immune response to
Fig. 24-7b
Second exposure
to antigen X,
first exposure
to antigen Y
Secondary immune
response to
antigen X
First exposure
to antigen X
Antibody concentration
Primary immune
response to
antigen X
Primary immune
response to
antigen Y
Antibodies
to X
Antibodies
to Y 7 14 21 28 35 42 49 56
Time (days)

30. Cell-mediated immunity
Cytotoxic T cells (Tc)
Effective against viruses, bacteria
Infected cells display antigens, and Tc binds to MHC/antigen combo
Stimulates production of more Tc
Costimulation by Th which were stimulated by macrophage display of antigens

31. Humoral immune response (secretion of antibodies by plasma cells)
Fig b
Humoral
immune
response
(secretion of
antibodies by
plasma cells)
Self-nonself
complex
B cell
Interleukin-2
stimulates
cell division
T cell
receptor 5 6 3
Interleukin-2
activates B cells
and other T cells 2
Helper
T cell 4 7
Cell-mediated
immune
response
(attack on
infected cells)
Antigen-presenting
cell
Cytotoxic
T cell
Interleukin-1
stimulates
helper T cell
Binding
site for
antigen
Binding
site for
self protein

32. Cytotoxic T cell binds to infected cell Self-nonself complex Foreign
Fig 1
Cytotoxic T cell binds
to infected cell
Self-nonself
complex
Foreign
antigen
Infected cell
Perforin
molecule
Cytotoxic
T cell

33. 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
Enzyme that
can promote
apoptosis
Cytotoxic
T cell

34. 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
Enzyme that
can promote
apoptosis
Cytotoxic
T cell

35. Show “Immune Response” Mcgraw Hill

36. Th stimulate both immune responses
Microbe
Macrophage
Self protein
Self-nonself
complex
T cell
receptor
Interleukin-2
stimulates
cell division
Interleukin-1
helper T cell
Binding
site for
antigen
self protein
Helper
Antigen-presenting
cell
Antigen from microbe
(nonself molecule) 1 2 3 4 5 6 7
B cell
Cytotoxic
Cell-mediated
immune
response
(attack on
infected cells)
activates B cells
and other T cells
Humoral
(secretion of
antibodies by
plasma cells)

37. Acquiring Adaptive immunity

38. Antigens, Antibodies & Vaccines
Inject host with inactive or attenuated virus (usually bits & pieces aka antigens)
Host immune cells grab antigens & stimulate other cells (B cells) to engineer antibodies to bind to antigens

39. Antigens, Antibodies & Vaccines
B cells “remember” how to make this antibody forever
On subsequent infection, live virus is mobbed by antibodies, targeted for termination and eaten by macrophages