Transcript Chapter 43 - cloudfront.net

Dispatch
1) Take out April calendar and pick up a book
-Today is the review (nut/lunch and afterschool)
-This Sat is the AP Exam #1 8-11 or Wed, April 16 3-6
-Today we have reading quiz Chapter 43
2) Share with your tablemates what you did during
break. Combine what all members did in one word
Example: Magicbeachshopping
3) Study notes chapter 43
Ms. Morris went to Zion, Utah
Chapter 43 ~
phagocytes
• The Body’s
Defenses
lymphocytes
attacking
cancer cells
Exit Quiz
1.
2.
Explain the inflammatory response
What are the main advantages and disadvantages of a physical barrier
against infection?
3.
Sketch a B-cell receptor. Label V + C regions of light and heavy chains.
Mark positions of antigen-binding sites, disulfide bridges and
transmemebrane regions.
4.
If a child were born without a thymus what cells and functions would be
deficient. Explain.
5.
HIV targets include all of the following EXCEPT:
A Macrophage
B Cytotoxic T-cells
C Helper T-cells
D Brain cells
Exit Quiz Answers
1) The inflammatory response (inflammation) occurs when tissues are injured
by bacteria, trauma, toxins, heat, or any other cause. The damaged cells
release chemicals including histamine, bradykinin, and prostaglandins.
These chemicals cause blood vessels to leak fluid into the tissues,
causing swelling. This helps isolate the foreign substance from further
contact with body tissues.
•
The chemicals also attract white blood cells called phagocytes that
"eat" microorganisms and dead or damaged cells. This process is called
phagocytosis. Phagocytes eventually die. Pus is formed from a
collection of dead tissue, dead bacteria, and live and dead phagocytes.
2) What are the main advantages and disadvantages of a physical barrier against infection?
A physical barrier often provides a very effective defense against infection. However it is
necessarily incomplete because animals need openings in their bodies for exchange with the
environment.
3) Sketch a B-cell receptor. Label V + C regions of light and heavy chains.
Mark positions of antigen-binding sites, disulfide bridges and transmemebrane regions.
4) If a child were born without a thymus he/she would not have functional T-cells. Without helper
T-cells to help activate B-cells, child would be unable to produce antibodies against
bacteria. Without T-cells or helper t-cells the child would be unable to kill viruses.
5) HIV targets include all of the following EXCEPT:
B Cytotoxic T-cells
Lines of Defense
Nonspecific Defense Mechanisms……
1st line: Non-specific External defense
• Barrier
• skin
Lining of trachea:
ciliated cells & mucus
secreting cells
• Traps
• mucous membranes, cilia,
hair, earwax
• Elimination
• coughing, sneezing, urination, diarrhea
• Unfavorable pH
• stomach acid, sweat, saliva, urine
• Lysozyme enzyme
• digests bacterial cell walls
• tears, sweat
2nd line: Non-specific patrolling cells
• Patrolling cells & proteins
bacteria
– attack pathogens, but don’t
“remember” for next time
• leukocytes
– phagocytic white blood cells
– macrophages, neutrophils, natural
killer cells
• complement system
macrophage
– proteins that destroy cells
• inflammatory response
– increase in body temp.
– increase capillary permeability
– attract macrophages
yeast
Leukocytes: Phagocytic WBCs
• Attracted by chemical signals released by damaged
cells
– ingest pathogens
– digest in lysosomes
• Neutrophils
– most abundant WBC (~70%)
– ~ 3 day lifespan
• Macrophages
– “big eater”, long-lived
• Natural Killer Cells
– destroy virus-infected cells
& cancer cells
Destroying cells gone bad!
• Natural Killer Cells perforate cells
– release perforin protein
– insert into membrane of target cell
– forms pore allowing fluid to
flow in & out of cell
natural killer cell
– cell ruptures (lysis)
vesicle
perforin
cell
membrane
perforin
punctures
cell membrane
cell
membrane
virus-infected cell
Anti-microbial proteins
• Complement system
– ~20 proteins circulating in blood plasma
– attack bacterial & fungal cells
• form a membrane attack complex
• perforate target cell
• apoptosis
extracellular fluid
– cell lysis
complement proteins
form cellular lesion
plasma membrane of invading
microbe
complement proteins
bacterial cell
Inflammatory response
• Damage to tissue triggers local
non-specific inflammatory
response
– release chemical signals
• histamines & prostaglandins
– capillaries dilate, become
more permeable (leaky)
• delivers macrophages, RBCs, platelets,
clotting factors
– fight pathogens
– clot formation
– increases temperature
• decrease bacterial growth
• stimulates phagocytosis
• speeds up repair of tissues
Fever
• When a local response is not enough
– system-wide response to infection
– activated macrophages release interleukin-1
• triggers hypothalamus in brain to readjust body thermostat to raise
body temperature
– higher temperature helps defense
• inhibits bacterial growth
• stimulates phagocytosis
• speeds up repair of tissues
• causes liver & spleen to store
iron, reducing blood iron levels
– bacteria need large amounts
of iron to grow
Dispatch
1) Draw a label a heart
2) How is 02 transported to mitochondria?
3) How is CO2 transported from mitochondria?
This Sat in this room. Be here at 7:50 am. Part I 100
multiple choice in 1.5 hours. Part II 4 FRQs
If your name is on the board, clear up your N
FLT
• I can compare the circulatory
system and the urinary system
with the skeleton baby
-Heart
-1 Artery along arm
-1 Vein along arm
-Urinary system (kidney, urethra, ureter,
bladder)
Immune System Play
• While actors are practicing, copy immune
chart pg 848
After play
1) Fill in the T-chart with 3 or more difference
between a bacteria and virus.
2) A B-cell has antibodies. These antibodies
are used to______________________
3) The role of a T-cell is to__________
4) What is the first line of defense our body has
against pathogens?______________
5) How is a virus attack handled differently than
a bacterial attack by the body?_______
3rd line: Acquired (active) Immunity
• Specific defense with memory
– lymphocytes
• B cells
• T cells
– antibodies
• immunoglobulins
• Responds to…
– antigens
• cellular name tags
– specific pathogens
– specific toxins
– abnormal body cells (cancer)
B cell
How are invaders recognized?
• Antigens
– cellular name tag proteins
• “self” antigens
– no response from WBCs
• “foreign” antigens
– response from WBCs
– pathogens: viruses, bacteria, protozoa, parasitic worms, fungi,
toxins
– non-pathogens: cancer cells, transplanted tissue, pollen
“self”
“foreign”
Lymphocytes
• B cells
– mature in bone marrow
– humoral response system
• “humors” = body fluids
• attack pathogens still circulating
in blood & lymph
– produce antibodies
• T cells
– mature in thymus
– cellular mediated system
• attack invaded cells
• “Maturation”
– learn to distinguish “self”
from “non-self” antigens
• if react to “self” antigens, cells
are destroyed during maturation
bone marrow
B cells
• Attack, learn & remember pathogens circulating in
blood & lymph
• Produce specific antibodies
against specific antigen
• Types of B cells
– plasma cells
• immediate production of antibodies
• rapid response, short term release
– memory cells
• continued circulation in body
• long term immunity
Y
Y
Y
Y
Y
antigen
Y
Y
• “this is foreign…gotcha!”
antigenbinding site on
antibody
Y
Y
– tagging “handcuffs”
Y
Y
• millions of antibodies respond to millions of
foreign antigens
Y
– multi-chain proteins
– binding region matches molecular shape of antigens
– each antibody is unique & specific
Y
Y
• Proteins that bind to a specific antigen
Y
Y
Y
Antibodies
Y
Y
Y
Y
Y
variable
binding region
each B cell
has ~50,000
antibodies
Y
Y
Y
Structure of antibodies
Y
s
s
s
light
chain
B cell
membrane
s
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s s
s s
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s
variable region
s
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s
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s
Y
Y
antigen-binding site
light
chain
heavy
chains
light chains
antigen-binding
site
heavy chains
antigen-binding
site
10 to 17 days for full response
Y
B cell immune response
Y
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release antibodies
Y
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plasma cells
recognition
Y
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macrophage
Y
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captured
invaders
Y
Y
Y
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Y
“reserves”
Y
memory cells
Y
B cells + antibodies
Y
Y
Y
invader
(foreign antigen)
Y
Y
tested by
B cells
(in blood & lymph)
Y
clones
1000s of clone cells
Induction of Immune Responses
• Primary immune response: lymphocyte proliferation and differentiation
the 1st time the body is exposed to an antigen
• Plasma cells: antibody-producing effector B-cells
• Secondary immune response: immune response if the individual is
exposed to the same antigen at some later time~ Immunological memory
Vaccinations
• Immune system exposed
to harmless version of pathogen
– stimulates B cell system to produce
antibodies to pathogen
• “active immunity”
– rapid response on future exposure
– creates immunity
without getting
disease!
• Most successful
against viruses
What if the attacker gets past the B cells in
the blood & actually infects (hides in)
some of your cells?
You need trained assassins to recognize &
kill off these infected cells!
Attack
of the
Killer T cells!
T
2007-2008
But how do T cells
know someone is
hiding in there?
How is any cell tagged with
antigens?
• Major histocompatibility (MHC) proteins
– proteins which constantly carry bits of cellular material from
the cytosol to the cell surface
– “snapshot” of what is going on inside cell
– give the surface of cells a unique label or “fingerprint”
MHC protein
Who goes there?
self or foreign?
T or B
cell
MHC proteins
displaying self-antigens
How do T cells know a cell is
infected?
• Infected cells digest some pathogens
– MHC proteins carry pieces to cell surface
• foreign antigens now on cell membrane
• called Antigen Presenting Cell (APC)
– macrophages can also serve as APC
• tested by Helper T cells
infected
cell
WANTED
MHC proteins displaying
foreign antigens
TH cell
T cell with antigen
receptors
T cells
• Attack, learn & remember pathogens hiding in
infected cells
– recognize antigen fragments
– also defend against “non-self” body cells
• cancer & transplant cells
• Types of T cells
– helper T cells
• alerts rest of immune system
– killer (cytotoxic) T cells
• attack infected body cells
– memory T cells
• long term immunity
T cell attacking cancer cell
T cell response
APC:
infected cell
recognition
helper
T cell
helper
T cell
helper
T cell
Y
Y
Y
Y
Y
Y
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Y
Y
Y
Y
Y
Y
recognition
Y
Y
helper
T cell
Y
clones
Y
APC:
activated
macrophage
stimulate
B cells &
antibodies
Y
interleukin 1
or
activate
killer T cells
Y
helper
T cell
killer
T cell
Attack of the Killer T cells
• Destroys infected body cells
– binds to target cell
– secretes perforin protein
• punctures cell membrane of infected cell
vesicle
Killer T cell
Killer T cell
binds to
infected cell
cell
membrane
infected cell
destroyed
perforin
punctures
cell membrane
target cell
cell
membrane
Abnormal immune function I
• Allergies
• hypersensitive responses to
environmental antigens
(allergens); mast cells release
histamine causes dilation and
blood vessel permeability,
epinephrine
• Antihistamines can relieve
symptoms
anaphylactic shock: life
threatening reaction to injected
or ingested allergens.
Abnormal immune function II
• Autoimmune disease:
– The system turns against
the body’s own
molecules
• Examples: multiple
sclerosis, lupus, rheumatoid
arthritis, insulin-dependent
diabetes mellitus
Rheumatoid arthritis
Abnormal immune function III
• Immunodeficiency disease:
•
Immune components are lacking, and infections recur
• Ex: SCIDS Severe combined immunodeficiency
Acquired Immunodeficency syndrome
(bubble-boy); A.I.D.S.,
Abnormal immune function IV
• Human Immunodeficiency
Virus
– virus infects helper T cells
• helper T cells don’t activate rest
of immune system: killer T cells
& B cells
• also destroys helper T cells
• AIDS: Acquired
ImmunoDeficiency Syndrome
– infections by opportunistic
diseases
– death usually from
– “opportunistic” infections
• pneumonia, cancers
HIV infected T cell