BIOL 191 Introductory Microbiology
Exam 4 Study Guide
Chap. 17 Adaptive Immunity: Specific Defenses of the Host
YouTube Basic Immunology Nuts and Bolts of Immunity (from ~30 minutes to the end)
Adaptive Immunity: Our Most Powerful Defense
 There are zillions of different B and T cells in your body, each created by chance to recognize one
thing (it may or may not ever come across this one thing). These ‘things’ are antigens (antibody
generators). They are specific for one antigen because each specific B and T cell has one type of
antigen receptor on its surface that recognizes (by being able to bond to it) one specific ‘foreign’
substance. The text estimates that we can respond to (a minimum of) 1015 antigens.
o B cells have receptors on their surface and secrete antibodies. Both the surface receptors
and antibodies can be referred to as immunoglobulins (abbrev. Ig). B cells may have
100,000 surface immunoglobulins on their surface.
o T cells have T-cell receptors (TCRs) on their surface and secrete cytokines.
Adaptive Immunity: Antibodies
 To understand how we create so many different kinds of B and T cells (so our immune system can
react to virtually anything foreign), you have to look at the DNA of a particular B or T cells during
its development. Fig. 17.8 Differentiation of T cells and B cells
o Stem cells in red bone marrow divide to form immature B cells or T cell.s This occurs in the
liver until about the third month of fetal development)
o The B cells continue to mature in the bone marrow
 During maturation (differentiation) the cell surface immunoglobulin receptor
structure and subsequent antibody structure for that B cell (and all B cells that
come from it through cell division) will be determined, purely by chance.
 In any one B cell, the immunoglobulin receptors and antibodies that will
be released bond to the same antigen- so they will have the same
antigen binding site structure. The cell surface immunoglobulin
receptors are basically antibodies that stick out of the cell surface while
other antibodies the B cell produces may be released into blood, lymph,
and other tissues and travel around the body.
 How is the structure of a given B cell’s immunoglobulins determined?
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o There are many possible genes in the DNA that can be used for
specific areas of the immunoglobulin (antibody). Fig. 17.3 The
structure of a typical antibody molecule
o For example, there are hundreds of ‘V’ genes that can be used in any
combination, while other V genes are not used. They are picked
randomly, purely by chance.
o V genes code for proteins that are found on the antigen binding sites
of the immunoglobulin. As a result of the random choosing of V
genes, random proteins that make up this area of the antibody will
be formed. These are the areas that vary among different B cells.
These variable areas of the immunoglobulin bond to a very specific
area of the antigen which is called the epitope (protein or large
polysaccharide or something combined with a protein or large
polysaccharide). Fig. 17.1 Epitopes (antigenic determinants)
o
Different B cells may bond to the same antigen, but different
epitopes on that antigen. They will not all have the same affinity for
the antigen- some bond better than others.
o The C (constant) genes code for proteins in the area of the
immunoglobulin that is the same in any one class of antibody (See
Table 17.1 for a summary of immunoglobulin classes). These so
called Fc regions of the antibody bond to other defensive cells
(phagocytes), complement, etc., not the antigen.
 Also during maturation, B cells that are reactive against ‘self’ molecules are
weeded out (clonal deletion).
o T cells undergo a similar maturation – they pick and choose which genes to use for their Tcell receptors (TCRs), but after they migrate to the thymus.
o After maturation, B and T cells migrate in the blood and lymph to lymphoid tissues where
they will be most likely to come into contact with antigens
 When a B cell surface immunoglobulin bonds to an antigen, it is activated to DIVIDE- CLONAL
SELECTION.
o Some of the daughter cells become plasma cells that may release antibodies which will
bond to the same antigen. These are the B cell plasma cells.
o
Some B cells produce antibodies against specific antigens on their own (Tindependent antigens)
o
Other B cells need T cells to activate them before they will form antibodies against
some antigens (T-dependent antigens) (Fig. 17.4 Activation of B cells to produce
antibodies). Fig. 17.4 Activation of B cells to produce antibodies (against a Tdependent antigen)
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o Some daughter cells become long-lived memory cells that do not release antibodies, but
will stay in the body (time varies, up to decades, for life?). -So your body is prepared to
react to the same antigen very quickly should it enter the body again- so quickly we may
not even notice the infection. This is the basis for VACCINATION.
o The strength of the bond between antigen and antibody will vary; the amount and
duration of the antibody production will also vary. The better the ‘fit’ between antigen
and antibody, the better the response.
o Fig. 17.7 The results of antigen-antibody binding. This figure illustrates how antibodies
work to protect our bodies
o The B cells and their antibodies are called humoral immunity
Adaptive Immunity: Antibodies II
 Fig. 17.18 Types of adaptive immunity
 Vaccines provide active immunity- the individual is making their own antibodies
 Passive immunity is acquired when antibodies are created by the mother or other animal and
given to the person.
 Polyclonal antibodies: come from many B cells; attach to different epitopes of the antigen
 Monoclonal antibodies: come from one type of B cell and attach to one epitope of the antigen
o Used in many therapies: cancers, immune system suppressors
Adaptive Immunity: Cell Mediated Immunity
 T cells are part of cell-mediated immunity (not humoral immunity)
 T cells are only activated when they recognize that another cell has had a foreign molecule inside
of them. This other cell is called an antigen presenting cell –APC. They must ‘present’ the
antigen to the T cell before it will react.
 The APC does this by…
o
First breaking up the antigen into fragments with enzymes (This occurs inside of the APC
so the antigen must be inside of the APC by being infected or actively transporting the
antigen into the APC).
Many pathogens that T cells fight are first recognized in the walls of
the intestinal tract. Therefore, lymphocytes and APCs are found just
under the epithelial-cell layer throughout the intestinal tract and
Peyer’s patches. B cells are also present in the gastrointestinal
lymphoid tissue. Many epithelial barriers have T and B cells in
them/just under them.
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o
MHC= Major
Histocompatibility
Complex. Also
known in humans
as HLA (Human
Leukocyte Antigen
system)
Then, one of the fragments of the antigen is combined with another molecule called
MHC (glycoproteins made by our cells and present in the APC previously).
o


The APC has been infected with the antigen itself (MHC I) or

The APC recognized the antigen outside of itself and brought it inside
(MHC II)
o
The APC combines its MHC with the antigen fragment
o
Then the APC inserts the MHC-antigen fragment complex in its cell membrane
so it is exposed to the outer environment
o
T cells that can also bond to that specific antigen fragment will be able to
recognize that the APC is showing them something foreign
o

The type of MHC depends on whether

The MHC II tells that T cells that see it that the APC is ‘self’ and is only
showing the other defensive cells that it has recognized something
foreign.

MHC I tells the T cells that this cell has been infected and this infected
cell needs to be destroyed
See * below for the next steps
APCs tend to migrate to lymphoid
tissues where they present the
antigen to the T cells located there.
APCs- Examples:
o
B cells
o
Dendritic cells
o
Activated macrophages
Types of T cells
o
Helper T cells (TH)
o
Also have special glycoprotein molecules called CD4 (they are CD4+ cells)- Bond
to MHC II on B cells and APCs

o
CD molecules help the T cell adhere to receptors
*Fig. 17.10 Activation of CD4+ TH

2 stimulations required
o
T cell bonding to MHC-antigen complex on the APC causes the
APC to release a cytokine (a costimulatory cytokine)
o
The cytokine released by the APC causes the CD4+ TH to release
its own cytokines which cause a slew of things, including…
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o
o

The CD4+ TH divides like crazy, producing different,
specialized CD4+ TH cells against different types of
infections, which then produce more specific cytokines
against specific types of infections (See Fig. 17.11)

Also produces TH memory cells.

B cells undergo clonal expansion and produce tons of
antibodies (see effects of antibodies Fig. 17.7)

Enhance the abilities of phagocytes to phagocytize and
present antigens.
Cytotoxic T cells (TC or CTL)
o
Have special glycoprotein molecules called CD8 (they are CD8+ cells)- Bond to
MHC I
o
Mostly kills cells that have been infected with a virus after a sequential and
complex set of interactions in which they bond to MHC I-antigen complex, drill a
hole in the cell and release granzymes that cause apoptosis
Regulatory T cells (Treg)- Suppress immune responses: get rid of T cells that recognize self
and those bacteria that are normal flora (and maybe the fetus)
o
A subset of CD4+ helper T cells
o
Release cytokines that inhibit immune responses
Natural Killer Cells

Don’t react to antigens but instead react to ‘self’ cells that do not have the normal ‘self’
MHC marker molecules (or too few or abnormal)

Form pores in the target cell

Imp. in destroying cancerous cells, virally infected cells, large parasites (worms)

Can be helped by antibody opsonization (NK cells may attach to the Fc region of antibodies
that have also bonded to an antigen with the antigen-binding sites.
Cytokines

Interleukins (IL): Communicators; stimulate activities of other defensive cells and the
cell that released it

Chemokines: Function in chemotaxis to induce migration to sites of infection of damage
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
Interferons (INF): Interfere with infections, for example viral infections

Tumor necrosis factor (TNF): Induces inflammation, can cause autoimmune diseases
(rheumatoid arthritis)

Hematopoietic cytokines: Control which type of differentiated blood cells are produced
from stem cells in red bone marrow (some are interleukins)
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