Biology: Seventh Edition
Unit 7: Animal Form and Function
Chapter 43: The Immune System
Adapted from Notes by: Jessica Liu
1)
2)
Innate immunity provides broad defenses against infection
a.
External Defenses
i.
Intact skin
ii.
Mucous membranes. Mucus—viscous fluid that traps microbes and other
particles
iii.
Secretions- Acidic environment of skin and stomach destroys many microbes
and pathogens
*.
Lysozyme—enzyme that digests the cell walls of many bacteria; present saliva,
tears, and mucous secretions; destroy bacteria as they enter upper respiratory
tract and openings around eyes
b.
Internal Cellular and Chemical Defenses
*.
Phagocytosis—the ingestion of invading microorganisms by certain types of white
blood cells [phagocytes] that produce antimicrobial proteins and help initiate
inflammation to limit spread of microbes
ii. Phagocytic Cells
1.
Attach to microbes via surface receptors that bind to structures found
on microorganisms but not in body cells
2.
Engulfs microbes, forming vacuole that fuses with lysosome; toxic
forms of oxygen e.g. nitric oxide moison microbes; lysozyme and other
enzymes degrade microbial components
iii.
Antimicrobial Proteins
1.
Complement system—made up of ~30 serum proteins; in the absence
of infection, are inactive; substances on surface of microbes trigger
activation, leading to lysis of invading cells; help trigger inflammation,
play role in acquired defense
2.
Interferon—α and β: secreted by virus-infected body cells; induce
neighboring uninfected cells to produce substances to inhibit viral
reproduction; interferon γ: helps activate macrophages
iv.
Inflammatory Response
1.
Inflammatory response—triggered by injury or entry of pathogens
2.
Histamine—trigger dilation and increased permeability of nearby
capillaries, promoting blood flow and inflammation and swelling [from
leaking fluid]
3.
Mast cells—found in connective tissues; cells in which histamine is
stored
4.
Inflammation helps deliver antimicrobial proteins and clotting
elements to injured area, beginning repair process and blocking spread
of microbes to other parts of body
5.
Chemokines—direct migration of phagocytes and signal them to
increase production of microbe-killing compounds; secrete by blood
vessel endothelial cells at or near site of injury or infection
v.
Natural Killer Cells
1.
Natural killer (NK) cells—attack virus-infected body cells and
cancer cells; surface receptors recognize general features on surface of
targets; releases chemicals the lead to death of cell by apoptosis
2.
Apoptosis—programmed cell death
In acquired immunity, lymphocytes provide specific defenses against infection
a.
Cytokines—proteins that help activate lymphocytes and other cells of immune system
b.
Antigen—usually proteins or polysaccharides; recognized by lymphocytes as foreign
and elicits response from lymphocytes; dissolved in extracellular fluid, protrude from
surface of foreign cells
c.
Epitope (antigenic determinant)—small, accessible portion of antigen to which
lymphocyte binds
d.
Antigen Recognition by Lymphocytes
i. Two main types of lymphocytes: B lymphocyte (B cell); T lymphocyte (T
cell)
3)
ii.
Circulate through blood, concentrated in spleen, lymph nods, lymphoid
tissues;
iii.
Antigen receptors—antigen-specific receptors in plasma membrane of
lymphocyte; all of ~100,000 on a cell are identical—specificity for epitope on an
antigen and defends against that antigen and closely related antigens
iv.
B Cell Receptors for Antigens
1.
B Cell receptor (membrane antibodies, membrane
immunoglobulins)—Y-shaped molecule consisting of four polypeptide
chains: two heavy chains [identical], two light chains linked by
disulfide bridge
2.
Transmembrane region anchors receptor in plasma membrane, short
region of tail extends into cytoplasm
3.
Variable (V) regions—regions at tips of Y light and heavy chains;
vary from one B cell to another; form antigen-binding site
4.
Constant (C) regions—everything not in V region; almost the same
in all cells
5.
Bonding between antigen binding site and antigen by noncovalent
bonds between chemical groups
v.
T Cell Receptors for Antigens and the Role of the MHC
1.
T cell receptor—consists of α-chain, β-chain linked by disulfide
bridge; transmembrane region anchors molecule in plasma membrane;
V regions for single antigen-binding site; recognize fragments of
antigens bound to normal MHC surface proteins
2.
Major histocompatibility complex (MHC)—family of genes that
codes for MHC molecule, which performs antigen presentation
a.
Class I MHC molecules—found on almost all nucleated
cells of body; bind peptides from foreign antigens that have
been synthesized within cell e.g. in cancer cells; when bound
to antigens, are recognized by cytotoxic T cells
b.
Class II MHC molecules—made by dendritic cells,
macrophages, B cells; bind peptides derived from foreign
material that have been internalized or fragmented through
pagocytosis or endocytosis; antigen-presenting cells—
dendritic cells, macrophages, B cells; display internalized
antigens to helper T cells
3.
Antigen Presentation—MHC molecule binds with fragment of
protein antigen within cell and brings it to cell surface as it moves
toward plasma membrane
4.
Because of many different MHC alleles, most people are
heterozygous for all MHC genes and can produce broad array of MHC
molecules; two people unlikely to have same set of MHC
molecules  chemical fingerprint of individual; marks cells as “self”
e.
Lymphocyte Development
i. Thymus—gland in thoracic cavity above heart where lymphocytes develop
to T cells
ii.
B cells mature in bone marrow
iii.
Clonal Selection of Lymphocytes
1.
“Selection” of B cell or T cell by antigen activates lymphocyte and
causes it to divide, forming two clones of daughter cells
2.
Effector cells—combat antigen; short-lived
3.
Memory cells—bear receptors specific for same inducing antigen;
long-lived
4.
Clonal selection—antigen-driven cloning of lymphocytes
5.
Primary immune response—proliferation of lymphocytes the first
time the body is exposed to a particular antigen; peak 10 to 17 days
after initial exposure
6.
Plasma cells—antibody-secreting effector B cells
7.
Secondary immune response—faster, more prolonged response the
second time the body is exposed to antigen
8.
Immunological memory—immune system’s ability to generate
secondary immune response; depends on clones of memory T and B
cells
Humoral and cell-mediated immunity defend against different types of threats
a.
b.
c.
d.
e.
f.
Humoral immune response—activation and clonal selection of B cells
Cell-mediated immune response—activation and clonal selection of cytotoxic T cells
Helper T cell—responds to peptide antigens displayed on antigen-presenting cells and
stimulates activation of B cells and cytotoxic T cells
Helper T Cells: A Response to Nearly All Antigens
i. Helper T cell recognizes class II MHC molecule-antigen complex on antigen
presenting cell proliferates into active helper T cell clone and memory helper
T cell
ii.
CD4—binds class II MHC molecule to keep helper T cell and antigenpresenting cell joined while activation of helper T cell proceeds
iii.
Active helper T cells secrete cytokines that stimulate other lymphocytes to
promote humoral and cell-mediated response
iv. Naïve helper T cells—helper T cells that have not yet detected antigen;
v. Macrophages present antigens to memory T cells; B cells present antigens to
helper T cells in humoral response
Cytotoxic T Cells: A Response to Infected Cells and Cancer Cells
i. Cytotoxic T cells eliminate infected body cells
ii.
Nonself proteins synthesized in target cells associate with class I MHC
molecule and are displayed on cell surface to be recognized by cytotoxic T cell
iii.
CD8—binds to class I MHC molecule keeps target cell and cytotoxic T
cell in contact during activation of cytotoxic T cell
iv.
When cytotoxic T cell binds to MHC molecule-antigen complex it
differentiates and becomes active killer; process promoted by cytokines from
nearby helper T cells
v.
Activated cytotoxic T cell secretes proteins that lead to its destruction
vi.
Perforin—forms pores in target cell membrane
vii.
Granzyme—proteolytic enzyme that enters target cell by endocytosis;
initiate apoptosis and lead to fragmentation of nucleus  release of apoptotic
bodies
B Cells: A Response to Extracellular Pathogens
i. B cell takes in antigen from surface of B cell by endocytosis and presents it
to helper T cell; T cell bearing receptor for antigen bind to B cell, secrete
cytokines to activate B cell
ii.
B cell stimulated by antigen and cytokines proliferates and differentiates
into clone of plasma cells and memory B cells
iii.
Macrophage and dendritic cell can present peptide fragments from wide
variety of antigens, but B cell binds and presents only antigen to which it
specifically bonds
iv. T-dependent antigens—antigens that induce antibody production only with
assistance from helper T cells
v.
T-independent antigens—can evoke B cell response without involvement of
helper T cells; e.g. polysaccharides of many bacterial capsules, proteins from
bacteria flagella; generally weaker response, no memory B cells
vi.
Antibody Classes
1.
Immunoglobulins
a.
IgM (pentamer)—first Ig class produced after initial
exposure to antigen, then concentration declines; promotes
neutralization and agglutination of antigens; effective in
complement activation
b.
IgG (monomer)—most abundant in blood, present in tissue
fluid; only Ig class that crosses placenta, confers passive
immunity on fetus; promotes opsonization, neutralization,
agglutination of antigens, less effective in complement
activation
c.
IgA (dimer)—present in secretions; provides localized
defense of mucous membranes by agglutination and
neutralization of antigens; J-chain + secretory component
d.
IgE (monomer)—triggers release of histamine from mast
cells and basophils that cause allergic reactions
e.
IgD—present on surface of naïve B cells that have not been
exposed to antigens; acts as antigen receptor in clonal
selection of B cells
vii.
Antibody-Mediated Disposal of Antigens
1.
4)
5)
Binding of antibodies to antigens inactivates antigens by:
a.
Viral neutralization—block binding to host; opsonization—
increases phagocytosis by increasing macrophage attachment
to microbes
b.
Agglutination—clumping of antigen bearing particles,
possible because each antibody molecule has at least 2 antigen
binding sites that can bind to identical epitopes on different
particles to link them together
c.
Precipitation—antibodies cross-link soluble antigen
molecules; form immobile aggregate
d.
Membrane attack complex (MAC)—forms pore in
membrane, cause cell to swell and lyse when complement
system activated
2.
Neutralization, opsonization, agglutination, precipitation enhance
phagocytosis
3.
Activation of complement system causes cell lysis
g.
Active and Passive Immunization
i. Active immunity—immunity conferred by natural exposure to infectious
agent; depends on activation of person’s own lymphocytes and resulting
memory cells
ii.
Immunization (vaccination)—develops active immunity; include
inactivated bacterial toxins, killed microbes, weakened microbes to induce
immediate immune response and immunological memory through memory
cells  quick secondary response
iii. Passive immunity—achieve immunity by transfer antibodies from
immune individual to non-immune individual; does not result from action of
recipient’s B and T cells; antibodies received immediately help destroy microbes;
last only as long as transferred antibodies live; occurs naturally in transfer of
antibodies from mother to child to protect infant against infection while their
immune system is maturing; occurs artificially in treatment of rabies
The immune system’s ability to distinguish self from nonself limits tissue transplantation
a.
Blood Groups and Transfusions
i. A type blood: Anti-B antibodies; B type: Anti-A; AB type: No anti-A or
anti-B; O type: Anti-A and Anti-B
ii.
O is universal donor; AB is universal recipient
iii.
Antigens against foreign blood type present even in absence of exposure
to foreign blood type because antibodies arise in response to normal bacterial
inhabitants of body
iv.
Anti blood group antibodies are always IgM; no memory cells generated
v.
Rh factor—induces immune response in which memory cells generated;
later exposure leads to anti-Rh IgG antibodies
Exaggerated, self-directed, or diminished immune responses can cause disease
a.
Allergies
i. Allergens—antigens that in exaggerated response cause allergies;
commonly involve IgE
ii.
Degranulation—mast cells release histamine and inflammatory agents
against pollen
iii.
Histamine increases permeability of small blood vessels
iv.
Antihistamines block histamine receptors
v.
Anaphylactic shock—whole-body, life-threatening reaction; occurs when
widespread degranulation by mast cells causes blood vessel dilation, sudden
drop in blood pressure; can be countered by epinephrine
b.
Autoimmune Diseases
i. Autoimmune diseases—immune system turns against self
ii.
Autoimmune disease arise from failure in immune system regulation
c.
Immunodeficiency Diseases
i. yeah like AIDS and stuff.