220 BISC General Biology
Cell Biology and Physiology
Instructor for Part 2
Michael Jakowec, PhD
[e-mail]
Lab: MCA-241 (HSC Campus)
Office Hours: ?
Q & A: Hedco 100 Thursday 2 to 3 pm
Date
Day
Lecture No.
Topic
Mar 3
Thurs
16
Cardiovascular System 1: Heart
Mar 8
Tues
17
Cardiovascular System 2: Blood System
Mar 10
Thurs
18
Respiratory System
Mar 11 Friday Exam Lectures 9 to 16
Mar 15 and 17 Optional Spring Break (Studying of course)
Mar 22
Tues
19
Immunity 1
Mar 24
Thurs
20
Immunity 2
Mar 29
Tues
21
Fluid and electrolytic balance 1
Mar 31
Thurs
22
Fluid and electrolytic balance 2
Apr 5
Tues
23
Endocrine System 1
Apr 7
Thurs
24
Endocrine System 2
Apr 8 Friday Exam Lectures 17-23
Apr 12
Tues
25
Reproduction 1
Apr14
Thurs
26
Reproduction 2
Apr 19
Tues
27
Nervous System 1
Apr 21
Thurs
28
Nervous System 2
Apr 26
Tues
29
Motor System 1
Apr 28
Thurs
30
Motor System 2
May 10 Exam Lectures 24 -30
Lecture 20
Tuesday March 24
Immune System Part 2
Sections 43.3 to 43.4
Cinematic Study Guides
Fig. 43-2
Pathogens
(microorganisms
and viruses)
INNATE IMMUNITY
Recognition of traits
shared by broad ranges
of pathogens, using a
small set of receptors
Rapid response
ACQUIRED IMMUNITY
Recognition of traits
specific to particular
pathogens, using a vast
array of receptors
Slower response
Barrier defenses:
Skin
Mucous membranes
Secretions
Internal defenses:
Phagocytic cells
Antimicrobial proteins
Inflammatory response
Natural killer cells
Humoral response:
Antibodies defend against
infection in body fluids.
Cell-mediated response:
Cytotoxic lymphocytes defend
against infection in body cells.
Fig. 43-7
Interstitial fluid
Adenoid
Tonsil
Blood
capillary
Lymph
nodes
Spleen
Tissue
cells
Lymphatic
vessel
Peyers patches
(small intestine)
Appendix
Lymphatic
vessels
Lymph
node
Masses of
defensive cells
Fig. 43-9
Antigenbinding
site
Antigenbinding site
V
Antigenbinding
site
V
V
V
C
Disulfide
bridge
C
Light
chain
C
C
Variable
regions
V
V
Constant
regions
C
C
Transmembrane
region
Plasma
membrane
Heavy chains
chain
chain
Disulfide bridge
B cell
) B cell receptor
Cytoplasm of B cell
Cytoplasm of T cell
(b) T cell receptor
T cell
Fig. 43-10
Antigenbinding
sites
Epitopes
(antigenic
determinants)
Antigen-binding sites
V
C
C
C
V
C
V
V
Antibody A Antigen
Antibody B
Antibody C
Fig. 43-11
Top view: binding surface
exposed to antigen receptors
Antigen
lass I MHC
olecule
Antigen
Plasma
membrane of
infected cell
Fig. 43-12
Dendritic Cell
Macrophage
fected cell
Microbe
Antigenpresenting
cell
1 Antigen
associates
with MHC
molecule
ntigen
ragment
Antigen
fragment
1
lass I MHC
olecule
1
cell
ceptor
a)
2
2
Cytotoxic T cell
Class II MHC
molecule
T cell
receptor
2 T cell
recognizes
combination
(b)
Helper T cell
Fig. 43-13
DNA of undifferentiated B cell
V37
V38
V39
V40
1
J1 J2 J3 J4 J5 Intron
C
DNA deleted between randomly selected V and J
segments
DNA of differentiated B cell
V37
V38
V39 J5 Intron
C
Functional gene
2 Transcription
pre-mRNA
V39 J5 Intron
C
3 RNA processing
mRNA Cap
V39 J5
C
B cell receptor
Poly-A tail
V
V
V
4 Translation
V
C
C
Light-chain polypeptide
V
C
C
Variable
region
Constant
region
B cell
C
Fig. 43-14
Antigen molecules
B cells that
differ in
antigen
specificity
Antigen
receptor
Antibody
molecules
Clone of memory cells
Clone of plasma cells
Fig. 43-15
Primary immune response
to antigen A produces
antibodies to A.
Secondary immune response to
antigen A produces antibodies to A;
primary immune response to antigen
B produces antibodies to B.
Antibody concentration
(arbitrary units)
104
103
Antibodies
to A
102
Antibodies
to B
101
100
0
7
Exposure
to antigen A
14
21
28
35
42
Exposure to
antigens A and B
Time (days)
49
56
Fig. 43-16
Humoral (antibody-mediated) immune response
Cell-mediated immune response
Key
Antigen (1st exposure)
+
Engulfed by
Gives rise to
Antigenpresenting cell
+
Stimulates
+
+
B cell
Helper T cell
+
Cytotoxic T cell
+
Memory
Helper T cells
+
+
+
Antigen (2nd exposure)
Plasma cells
Memory B cells
+
Memory
Cytotoxic T cells
Active
Cytotoxic T cells
Secreted
antibodies
Defend against extracellular pathogens by binding to antigens,
thereby neutralizing pathogens or making them better targets
for phagocytes and complement proteins.
Defend against intracellular pathogens
and cancer by binding to and lysing the
infected cells or cancer cells.
Fig. 43-16a
Humoral (antibody-mediated) immune response
Key
+
Antigen (1st exposure)
Stimulates
Engulfed by
Gives rise to
Antigenpresenting cell
+
+
B cell
Helper T cell
+
Memory
Helper T cells
+
Plasma cells
+
Antigen (2nd exposure)
Memory +
B cells
Secreted
antibodies
Defend against extracellular pathogens
Fig. 43-16b
Cell-mediated immune response
Key
+
Antigen (1st exposure)
Engulfed by
Stimulates
Gives rise to
Antigenpresenting cell
+
+
Helper T cell
Cytotoxic T cell
+
Memory
Helper T cells
+
+
Antigen (2nd exposure)
+
Active
Cytotoxic T cells
Memory
Cytotoxic T cells
Defend against intracellular pathogens
Helper T-Cells
Enhance humoral and cell-mediated responses
Proliferate after interacting with antigen-presenting cell (dendritic cell)
Differentiates into activated helper cell and memory helper T cell
Secrete cytokines as cell signal APC and Helper T cell
Complex interaction of MHC II and CD4 (anchor)
Dendritic cell
Macrophage
B Cell
Cytotoxic T Cells
Effector cells of cell mediated response
Activated by interactions with Helper T cells and Antigen
presenting cell
Involve removal of infected cells
Recognize epitopes presented by MHC I
Major surface receptor CD8
Interaction of CD4+MHC II are similar to CD8+MHC I except
they involve different cell types (Helper TC and Cytotoxic
TC)
B Cells
Activated by antigens
and cytokines from
Helper T Cells
Presents only one type of
antigen (which it binds)
Activation leads to robust
humoral response
including antibody
production and clonal
selection
Where is everyone coming from?
Fig. 43-17
Antigenpresenting
cell
Peptide antigen
Bacterium
Class II MHC molecule
CD4
TCR (T cell receptor)
Helper T cell
Humoral
immunity
(secretion of
antibodies by
plasma cells)
Cytokines +
+
B cell
+
+
Cytotoxic T cell
Cell-mediated
immunity
(attack on
infected cells)
Fig. 43-18-1
Cytotoxic T cell
Perforin
Granzymes
CD8
TCR
ass I MHC
lecule
rget
ll
Peptide
antigen
Fig. 43-18-2
Cytotoxic T cell
Perforin
Granzymes
CD8
TCR
ass I MHC
lecule
rget
ll
Pore
Peptide
antigen
Fig. 43-18-3
Killing Action of Cytotoxic T Cells
Released cytotoxic T cell
Cytotoxic T cell
Perforin
Granzymes
CD8
TCR
ass I MHC
lecule
rget
ll
Dying target cell
Pore
Peptide
antigen
Release perforin (creates holes in membranes)
Granzymes (proteinases)
Fig. 43-19
B Cell activation of Humoral Immune Response
tigen-presenting cell
Bacterium
Peptide B cell
antigen
ss II MHC
lecule
TCR
Clone plasma of cells
+
CD4
Cytokines
Secreted
antibody
molecules
Endoplasmic
reticulum of
plasma cell
Helper T cell
Activated
helper T cell
Clone of memory
B cells
2 m
Induction of Ig production and establishing Immune Memory
Fig. 43-19-1
ntigen-presenting cell
Bacterium
Peptide
antigen
ss II MHC
lecule
TCR
CD4
Helper T cell
Fig. 43-19-2
ntigen-presenting cell
Bacterium
Peptide
antigen
B cell
ss II MHC
lecule
TCR
+
CD4
Helper T cell
Cytokines
Activated
helper T cell
Fig. 43-19-3
ntigen-presenting cell
Bacterium
Peptide
antigen
B cell
ss II MHC
lecule
TCR
Clone of plasma cells
+
CD4
Helper T cell
Cytokines
Activated
helper T cell
Clone of memory
B cells
Secreted
antibody
molecules
Fig. 43-19a
Endoplasmic
reticulum of
plasma cell
2 m
Fig. 43-20
Class of Immunoglobulin (Antibody)
Distribution
IgM First Ig class
produced after
(pentamer)
initial exposure to
antigen; then its
concentration in
the blood declines
J chain
Five
Immunoglobulin (Ig)
Classes
IgGMost abundant Ig
(monomer) in blood;
class
also present in
tissue fluids
Function
Promotes neutralization and crosslinking of antigens;
very effective in
complement system
activation
Promotes opsonization, neutralization,
and cross-linking of
antigens; less effective in activation of
complement system
than IgM
Only Ig class that
crosses placenta,
thus conferring
passive immunity
on fetus
IgA Present in
secretions such
(dimer)
as tears, saliva,
mucus, and
J breast milk
chain
Provides localized
defense of mucous
membranes by
cross-linking and
neutralization of
antigens
Presence in breast
milk confers
passive immunity
on nursing infant
Secretory
component
IgEPresent in blood
at low
(monomer) concentrations
IgD Present primarily
(monomer)surface of
on
B cells that have
not been exposed
to antigens
Transmembrane
region
Triggers release from
mast cells and
basophils of histamine and other
chemicals that cause
allergic reactions
Acts as antigen
receptor in the
antigen-stimulated
proliferation and
differentiation of
B cells (clonal
selection)
Fig. 43-20a
Class of Immunoglobulin (Antibody) Distribution
IgM
(pentamer)
J chain
First Ig class
produced after
initial exposure to
antigen; then its
concentration in
the blood declines
Function
Promotes neutralization and crosslinking of antigens;
very effective in
complement system
activation
Fig. 43-20b
Class of Immunoglobulin (Antibody) Distribution
IgG
(monomer)
Most abundant Ig
class in blood;
also present in
tissue fluids
Function
Promotes opsonization, neutralization,
and cross-linking of
antigens; less effective in activation of
complement system
than IgM
Only Ig class that
crosses placenta,
thus conferring
passive immunity
on fetus
Fig. 43-20c
Class of Immunoglobulin (Antibody) Distribution
IgA
(dimer)
J chain
Secretory
component
Present in
secretions such
as tears, saliva,
mucus, and
breast milk
Function
Provides localized
defense of mucous
membranes by
cross-linking and
neutralization of
antigens
Presence in breast
milk confers
passive immunity
on nursing infant
Fig. 43-20d
Class of Immunoglobulin (Antibody) Distribution
IgE
(monomer)
Present in blood
at low concentrations
Function
Triggers release from
mast cells and
basophils of histamine and other
chemicals that cause
allergic reactions
Fig. 43-20e
Class of Immunoglobulin (Antibody) Distribution
IgD
(monomer)
Transmembrane
region
Present primarily
on surface of
B cells that have
not been exposed
to antigens
Function
Acts as antigen
receptor in the
antigen-stimulated
proliferation and
differentiation of
B cells (clonal
selection)
Fig. 43-21
Functional Features of Immunoglobulins
Viral neutralization
Opsonization
Activation of complement system and pore formation
Bacterium
Complement proteins
Virus
Formation of
membrane
attack complex
Flow of water
and ions
Macrophage
Pore
Foreign
cell
Fig. 43-21a
Viral neutralization
Virus
Render pathogens
ineffective for
infection
Fig. 43-21b
Opsonization
Bacterium
Enhance presentation
of antigens to
macrophages for
phagocytosis
Macrophage
Fig. 43-21c
Activation of complement system and pore formation
Complement proteins
Formation of
membrane
attack complex
Flow of water
and ions
Pore
Foreign
cell
Antibodies as Lab Tools
Production of Polyclonal Antibodies
Antibodies as Lab Tools
Production of Monoclonal Antibodies
Fig. 43-22
Passive Immunity
Active Immunity
The dramatic 1796 experiment
used fluid taken from a
cowpox sore on milkmaid
Sarah Nelmes. The
experimental subject was 8year-old James Phipps, who
did not get smallpox despite
Jenner's repeated attempts to
infect him starting July 1.
Ethicists debate whether such an ex
Edward Jenner
Vaccination and Inoculation
Influenza
Smallpox
Diptheria
Pertussis (Whooping cough)
Tetanus
Typhoid
Measles
Mumps
Hepatitis
Chicken pox
Meningitis
Polio
Pneumonia
HIV
Fig. 43-23
Mast Cells, IgE, Allergic Response
IgE
Allergen
Histamine
Granule
Mast cell
Hypersensitive response to allergens
Mast cells release histamine, other components (granulation)
Antihistamines block Histamine receptors
Anaphylactic Shock (Anaphylaxis)
Respiratory or whole body mast
cell degranulation
Epinephrine injections (epi-pen)
Rhesus (Rh) Factor
Hemolytic disease of the
newborn
Antigenic factor discovered
by immunizing Rhesus
monkeys with rabbit serum
Immunological response by
mother against fetus
Leads to severe anemia and
organ injury in fetus or
newborn
Treat mother with anti-D
gamma globulin
Fig. 43-24
Autoimmune Disease
Rheumatoid Arthritis
Systemic inflammatory disorder attaching
the synovial joints leading to destruction
of articular cartridge.
Systemic Lupus Erythematosus
Systemic
Autoimmune Disease
Multiple Sclerosis
Organ and Tissue Transplant
MHC class I and II Alleles
Immunosuppression
Host versus Graft
Graft versus Host
Evading the Immune System
Antigenic Variation
Latency
Direct Attack
Antigenic Variation
Influenza Virus
Antigenic Variation (Trypanosomes)
Fig. 43-25
Millions of parasites
per mL of blood
1.5
1.0
Antibodies to
variant 1
appear
Variant 1
Antibodies to Antibodies to
variant 2
variant 3
appear
appear
Variant 2
Variant 3
0.5
25
0
26
27
Weeks after infection
28
Latency
Herpes Simplex Virus
Human Immunodeficiency Virus (HIV)
Attacking the Immune System
Fig. 43-26
AIDS
Latency
Helper T cell concentration
in blood (cells/mm3)
800
600
400
Relative antibody
concentration
Relative HIV
concentration
Helper T cell
concentration
200
0
0
1
2
3
4
5
6
7
8
Years after untreated infection
9
10
HIV/AIDS
Karposis Sarcoma
Neural
Atrophy
Pneuomocystic carinii
Saccharomyces
Yeast
Harnessing the Immune System to
Fight Cancer
Maintaining Healthy Immune System
Exercise
Diet
Genetics
Stimulation
Fig. 43-UN1
Stem cell
Cell division and gene rearrangement
Elimination of
self-reactive
B cells
Antigen
Clonal selection
Formation of activated cell populations
Antibody
Memory cells
Effector B cells
Microbe
Receptors bind to antigens