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Transcript
The Immune System
AP Biology Exam Review
Organization of the Immune System

Nonspecific Immunity
 General defense against
anything “not self”
(MHC-I protein = “self”)

Primary cells: phagocytes
(like macrophages) that
“eat” invaders

Quicker

Specific Immunity
 Targets specific invader

Primary cells:
lymphocytes (T & B cells)

Slower, but builds
“memory”
Organization of the Immune System
Skin
Phagocytes
Mucous Membrane Fever
Secretions
Inflammation
Lymphocytes (B&T)
Antibodies
Nonspecific Immunity
Side note…
 Species Resistance

Why will you never catch
Dutch elm rot?

Why will an apple tree
never catch rabies?
Nonspecific Immunity
“1st line of defense” – physically &/or
chemically block entry!
 Mechanical Barriers

Skin & mucous membranes
physically block entry


This lines all outer surface
as well as inner barriers
Note: your digestive tube is
not “in” you (or respiratory, or…)
Nonspecific Immunity
“1st line of defense” – physically
&/or chemically block entry!
 Chemical Barriers




Oil & sweat on skin – creates low pH (non-native
microbes can’t survive); anti-fungal compounds
Saliva & tears – contain lysozyme (breaks cell walls)
Mucus – sticky to trap them; also has lysozyme
HCl in stomach – few microbes can survive this
Nonspecific Immunity
“2nd line of defense”
Phagocytosis
 Macrophages (& others) engulf invaders
 While they are nonspecific…they can help to
stimulate the specific mechanisms by
sounding the alarm
 Are APCs…antigen-presenting
cells (antigen = invader particle)
Nonspecific Immunity
“2nd line of defense”
Chemical Mechanisms
 Interferon
 Protein released by
virus-invaded cells
 Chemical interferes with
virus’ ability to attach to
neighboring cells
Nonspecific Immunity
“2nd line of defense”
Chemical Mechanisms
 Complement
 Group of enzymes that
lyse cells
 Activated by specific or
nonspecific
Nonspecific Immunity
“2nd line of defense”
Inflammation
 Chemicals that stimulate inflammatory response:
histamine, prostaglandins, leukotrienes
 Increased blood flow & vessel permeability…
helps WBCs get to infection site to phagocytize
Overview of Specific Immunity
Types of Specific Immunity
1. Inherited (Innate) – genetic;
forms during gestation
- does not “last” as long
- includes species resistance
2. Acquired – after birth


Natural – form antibodies
after exposure
Artificial – vaccines allow
for antibody formation
Overview of Specific Immunity

Mechanisms
1. Humoral Immunity – has B cells
with antibodies for indirect attack
2. Cell-mediated Immunity – has
T cells with more direct attack
3. lymphocytes densest where they
develop: bone marrow, thymus,
lymph nodes, spleen
Specific Immunity
Humoral = fluid (blood)
Cell-Mediated= cells
Specific Immunity
Helper T-Cells (link btwn humoral & cell-mediated)

APCs (macrophages & some B’s) alert immune
system to the foreign antigen by using helper T’s
Specific Immunity
Helper T-Cells

Once activated, helper T’s secrete IL-2 (interleukin-2)
that stimulates B cells to become plasma cells AND
stimulates cytotoxic T cells to activate
Humoral Immunity (humor = fluid)
B-Cells develop in 2 stages
1. pre-B cells develop by few months of age
(“inactive B cells”)
2. stage two (activation) in lymph nodes & spleen
 Antigen binds to antibody receptor…they
clone selves
 Activated B = “plasma cells” (make antibodies)
 Some remain as “memory B cells”
Humoral Immunity
Humoral Immunity
Antibody Action
1. Plasma cells secrete
specific counterparts to
antigens, called antibodies
2. An antibody matches one specific antigen
 Bind with it & bend it together…incapacitates it
3. this also stimulates inflammatory response &
complement reactions
Humoral Immunity
Humoral Immunity
Antibody Structure & Function
1. Y-shaped; 4 polypeptide
chains (how many genes?)
2. C-region (constant) is same in
all antibodies
3. each chain topped with
variable regions …allows for
great diversity of antibodies
4. the epitope of the antigen
binds at V-region
Humoral Immunity
Antibody Structure & Function
5. There are 5 major classes of antibodies
(immunoglobulins) – do not memorize!





IgM – a pentamer; first to arrive on scene, so indicates
current infection; cannot cross placenta (?)
IgG – most abundant
IgA – made by mucous membrane cells; milk
IgD – found on B cells; do not cross into placenta (?)
IgE – attach to mast cells & basophils; stimulate
release of histamine in allergic reactions 
Cell-Mediated Immunity
A. T Cells Overview
1. these go thru thymus before
nodes or spleen
2. Provide “direct attack”
3. Harder to activate – need 2
signals (why?)
B. T Cell Activation & Function
1. T cells must recognize “self” AND
“nonself” at the same time to be activated
An APC uses the MHC-II to present antigen
(depending on cell type, it might be an MHC-I, but same idea!)
Cell-Mediated Immunity
B. T Cell Activation & Function
2. It displays specific antigen
receptor on own surface
3. an APC uses the MHC-II (or
other) to present antigen
…the T-cell binds with both
4. T cell divides, forming clones
…called “sensitized T cells”
5. sensitized T cells will either
be cytotoxic T cells or
memory T cells
Cell-Mediated Immunity
B. T Cell Activation & Function
6. other types of T cells:
 Suppressor T cells – suppress B cells from
turning into plasma cells
 Helper T cells – help B cells turn into plasma
cells (discussed earlier)
Can you tell
this story?
Side note…
HIV Infection – attacks the T cells
Can you
explain
the data
shown on
the
graph?
Review! Can you explain it?
Review! What does each do?
Review! Can you explain it?
Review! What’s going on here?
Review! What’s going on here?
The End
Free Response Practice
2014 #2 - Mammalian milk contains antibodies produced by the
mother’s immune system & passed to offspring during feeding.
Describe FOUR steps in the activation of the mother’s immune
response following exposure to a bacterial pathogen.
Predict
how the mother’s immune response would differ upon a
second exposure to the same bacteria a year later.
Predict
the most likely consequence for a nursing infant who is
exposed to an intestinal bacterial pathogen to which the mother
was exposed three months earlier.
Free Response Practice

Explain how the human immune system…
A. provides an immediate nonspecific immune response

B. activates T and B cells in response to an infection.

C. responds to later exposure to same infectious agent

D. distinguishes self from nonself

Unit 7 Test: FreeResponse Rubric
A. – NONSPECIFIC
1 – physical barrier that blocks entry

2
skin, mucous membrane; saliva, tears, etc
– chemical barrier prevents entry/damages

Low pH/high salt kill, oil antifungal, lysozyme bursts
– inflammation – with description of any effect
4 – chemical agents – prevent spread or kill
3

Interferon, pyrogens, histamine (with description)
– phagocytosis – engulf invader
6 – elaboration (2nd ex. of #1/ #2; complement, etc)
5
Unit 7 Test: FreeResponse Rubric
39. (B) – ACTIVATING T & B CELLS
1 – macrophages engulf/present antigens
2 – TH or TC activated by binding to APC
3 – B cell activated by binding to antigen
4 – B or TC activated by binding to TH
5 – OTHER
 TH secretes IL-2 to activate B or TC
 CD4 on TH or CD8 on TC – self/nonself binding
Unit 7 Test: FreeResponse Rubric
39. (C) – SECONDARY EXPOSURE
1 – mediated by memory cells
2 – memory cells specific to SAME previous antigen
3 – antibody production is now faster/higher
– memory cell origin (activated cells  memory cells)
5 – memory cells more numerous OR antibody # high
6 – OTHER???
4
Unit 7 Test: FreeResponse Rubric
39. (D) – SELF from NON-SELF
1 – all cells have unique ID tags (self tags; MHC-I)
2 – developmental selection – how cells tested to
ensure that attach nonself, but not attack self
– binding elicits the response (how it recognizes
self/nonself)
4 – OTHER???
3


Describe self/nonself incompatabilities (bood transfusion;
organ donation, etc)
Describe difference btwn MHC-I and MHC-II