The Immune System
Chapter 40
Primary Immune Response
This is how immunity to disease is acquired
Requires time
Two components
Recognition
Requires exposure to invading agent
Response
Involves a searching effort (clonal selection)
Secondary Immune Response
The response of the immune system to the
second or subsequent occasion on which it
encounters a specific antigen.
Lymphocytes
Primary
participants in the
immune response
Types of
lymphocytes: B-
cells and T-cells
Both originate in
red bone marrow
(stem cells)
Differentiation
Occurs in the Primary
Lymphoid Tissues
(thymus and spleen)
Lymphocytes develop
special recognition sites
on their membranes
B-cells
Differentiation occurs in
red marrow
T-cells
Differentiation occurs in
thymus
Migration
After differentiation, B-cells
and T-cells migrate to
Secondary Lymphoid
Tissues
Lymph nodes
Spleen
Adenoids
Tonsils
Peyer’s Patches: Intestinal
lining
MALT
Lymph Nodes
B-cells, T-cells, and
macrophages are “stored”
here
Lymph nodes receive fluid
from tissues and blood
May contain bacteria,
viruses, etc.
Brings lymphocytes in
contact with these invaders,
allows for immune response
B-cells secrete antibodies that
fight antigens
Antibodies (AKA immunoglobins)
are proteins that bind to specific
antigens
B-Cells
Antigen (AKA immunogen) is any
molecule that can stimulate the
immune response.
Protein, nucleic acid,
carbohydrate (5000+ u)
Free molecules or part of the
membrane of an invader
Antigenic determinants-localized
chemical groups that trigger the
formation of an antibodies
Virgin B-cells
Mature B calls equipped with
surface antibodies
Migrate to secondary lymphoid
tissue to await invaders
Structure of Antibody
4 polypeptide chains
2 heavy chains
2 light chains
Chains held together by disulfide
linkages
Y-shaped configuration
Variable regions
2 branches of the Y
Antigen binding Sites
Contained in variable region
Bind antibody to antigenic
determinant
Millions of varieties
Constant Region
Same in all antibodies in a given
class
Fc Regions
Contained in constant region
Make phagocytosis more
effective
Antibody Classes-Fig 40.11
IgG
IgA
IgM
IgD
IgE
Differ in structure, location, target, and action
5 Antibody-Antigen Interactions (figure 40.12 )
1. Neutralizing- antibodies encounter and surround free antigens, neutralizing
harmful chemical effects.
2. Activating Complement- When IgM and IgG bind to invaders, it activates
complement and causes the lysis of cells.
3. Viral binding- Antibodies bind to the host cell binding site on the virus,
rendering them harmless.
4. Bacterial binding- IgM is a pentamer (5 binding sites_so it can bind to lots of
bacteria at once and make phagocytosis by a phagocyte easier.
5. Opsonization- Multiple monomer antibodies bind to invader exposing many
constant regions making phagocytosis easier.
Major Histocompatibility Complex
(MHC)
T-Cells
Complex of genes found on
chromosome # 6
Determines our cell surface
proteins
2 MHC protein groups are important
here-MHC class I and MHC class II
Helps us recognize our own cells
as “self”
T-cells have recognition sites that
match MHC proteins, healthy cells
are ignored
Figure 40.13
Most body cells are coded as MHC
class I
T and B cells and macrophages are
coded as class I or II
Identification of Infected Cells by T-Cells
Infected cells incorporate antigenic material into MHC protein
T-cells have dual recognition sites
One recognizes MHC site (class I or II)
One recognizes antigens
Lots of variability in antigen site/T cells
Almost any antigen can be recognized
Figure 40.14
Cytotoxic T-cells (Tc, T8)
Recognize class I MHC proteins
Seek out and attack diseased body cells
Helper T-cells (T4, Th)
Recognize class II MHC proteins
Recognize T-cells, B-cells, and macrophages and interact with them
Coordinate Immune response
Virgin T-cells
Mature T-cells equipped with dual recognition sites
Migrate to secondary lymphoid tissue to await invaders
Primary Immune Response
Complex set of events
Occurs with first encounter w/new invader
(antigen)
Takes time
First Step—Clonal Selection
Immune cells with the correct antigen receptor must be
located
Those cells must multiply
Second Step--Response
Humoral or Cell-Mediated
Clonal Selection
Proliferation of clones from a
single line of lymphocytes-
This process takes time
because
1. cells bearing the correct
antigen receptor must be found
2. these cells must multiply
Involves Macrophage
Eat invaders including free
antigens
Have both classes of MHC’s
Role of Macrophages in Clonal Selection
Serve as an
intermediary trigger (T-
cells cannot be
activated by antigen)
Have both Class I and
Class II proteins on
their membranes
The Steps of Clonal Selection (see figure 40.17)
1. Macrophage eats invader.
2. Material from invader conserved to
make sites to bind with a T-cell.
3. Conserved materials from extra-cellular
pathogens (bacteria) incorporated into
the macro’s Class 2 proteins
4. Conserved materials from intra-cellular
pathogens (viruses) are incorporated
into the macro’s Class 1 proteins
5. Surface of macro becomes the
reciprocal of a T-cell dual recognition site
6. The macrophage is now known as an antigen-presenting cell
7. The antigen presenting cell bumpsinto virgin T-cells till it finds one whose
dual receptors form a match.
8. Because antigen presenting cells have both Class I and Class II MHC
proteins, they can match (bind) with both Tc and Th cells.
Spreading The Alarm-Aroused T-Cells (figure 40.18)
T cell and macrophage (antigen presenting cell)
bind causing macrophage to release a chemical
messenger called interleukin 1.
This makes the attached T-cell undergo many
cell divisions
When Th cells get aroused, they also release
interleukin 2 that causes Tc cells to divide even
more!
All of these new T-cells can recognize the
antigen that initiates the process.
A small number of these new T-cells are set
aside as memory cells
Tc cells –Cell Mediated Response
Role is to “frisk” every cell till it finds
a matching antigen.
Once a diseased cell is found the Tc
cell releases perforin (this chemical
makes holes in the infected cell
causing it to lyse.
Some Tc cells release lymphotoxin
(this chemical activates enzymes of
viruses to fragment their own DNA,
thus preventing the virus from
multiplying
Some release gamma-interferon
(this chemical stimulates phagocytes
to clear up cellular debris)
Can also fight cancer cells as long
as the cancer has not metastasized.
Th cells—Humoral Response (figure 40.20)
Two roles
1. increase cell division
2. activate B-cells
B-cells are aroused when the surface of
a virgin B-cell binds to a matching free
antigen.
B-cell takes in the free antigen then
makes class 2 MHC proteins
Then the B-cell matches and binds to a
Th cell.
The Th cell secretes interleukin 2
This chemical causes B-cells to multiply
(form clones)
Some clones set aside as memory cells
Once B-cell activated are called
plasma cells
These cells are short lived (4-5
days) but secrete up to 2000
antibody molecules per second!
See earlier discussion of antibodies
to remember the types of interactions
they have with antigens.
B-cells
Some B-cells don’t need to be
activated by Th cells
The B-cell randomly
encounters the antigen that
matches its MHC site
Antigen is taken in and triggers
B-cell to divide (no chemicals)
Vast array of clones are made
These type of B cells are very
limited
Suppressor T cells or Ts
Monitors the immune system and keeps
it from running out of control
Brings the Primary Immune response to a halt
after danger has passed.
These cells may inhibit remaining appropriate
virgin T and B cells.
Since their lives are short (T and B cells) Ts cells
only need to suppress for a short time.
Memory cells and the 2 o response
Some of the activated T and
B cells remain as memory
cells
If another invasion of the
same invaders occurs these
cells recognize them
immediately and start their
attack.
We may not even notice
that this is happening or the
symptoms are very mild