Chapter 22 Flashcards
immunity def (resistance)
ability to ward off damage or disease through our defenses
susceptibility def
vulnerability or lack of resistance
2 types of immunity
innate adaptive
innate immunity
non specific acts against all microbes the same way)
defenses present at birth
1st and 2nd line of defense
1st line of defense vs 2nd in innate immunity
the physical and chemical barriers of the skin and mucous membranes
antimicrobial substances, natural killer cells, phagocytes, inflammation, fever
adaptive immunity
specific response to specific microbe (adapts/adjusts)
lymphocytes (WBC), T cells B cells
body system responsible for adaptive immunity
lymphatic
lymphatic system components
lymph: interstitial fluid that passe through lymph vessels
lymphatic vessels
lymphatic tissues: specialized reticular CT with large # lymphocytes
red bone marrow
function of lymphatic system
drain excess interstitial fluid: drain and return to blood
transport dietary lipids: lipids and vit A,D,E,K from GI tract
carry out immune response: against specific microbes/abnormal cells
where are lymphatic capillaries found
everywhere except avascular tissues, CNS, portions of spleen, red bone marrow
lymphatic vs blood capillaries
L: greater permeability (absorb large molecules)/diameter, interstitial fluid can come in but not go out, more valves
lacteals
specialized lymphatic capillaries in SI carry dietary lipids into lymphatic
vessels and ultimately into the blood (chyle)
lymph from SI vs everwhere else
called chyle and is creamy white
lymph and is clear pale yellow
lymph trunks are
lymphatic vessels exit lymph nodes in a particular region of the body, they unite to form lymph trunks
AKA: Small lymphatic vessels join together to form trunks
principal lymph trunks
lumbar, intestinal,bronchomediastinal, subclavian, and jugular trunks
bronchimediastinal trunks drain
thoracic wall lung heart
subclavian trunk drains
upper limbs
how does lymph enter superior vena cava
upper right quadrant returns vis right brachiocephalic veins
everywhere else via left brachiocephalic vein
pumps that maintain flow of lymph
respiratory pump
skeletal muscle pump
respiratory pump
inhale= lymph from abdomen to thoracic region
exhale=valves prevent backflow
skeletal muscle pump
milking action forces lymph toward the junction of the internal jugular and subclavian veins
primary lymphatic organs (def,what)
are the sites where stem cells divide and become immunocompetent (capable of mounting an immune response)
red bone marrow: B cells, pre-T cells
thymus: pre-t cells become T cells
secondary lymphatic organs (def,what)
sites where most immune responses occur
lymph nodes, the spleen, and lymphatic nodules
why are lymphatic nodules (follicles) not organs
lackl a CT capsule
capsule of thymus
one surrounding whole thing and one surrounding each lobe
trabeculae of thymus
extensions of the capsule and penetrate and divide each lobe into lobules
cortex of thymus
darkly staining
composed of large numbers of T cells and scattered dendritic cells, epithelial cells, and macrophages (clear out debris)
pre-t cells travel from RBM and mature here
medulla of thymus
light staining
consists of widely scattered, more mature T cells, epithelial cells, dendritic cells, and macrophages
some epithelial cells filled with keratin=thymic (Hassall’s) corpuscles.
thymic (Hassall’s) corpuscles.
epithelial cells in thymus medulla that degenerate and become filled with keratohyalin granules and keratin
may serve as sites for t cell death
functional mass of thymus as baby vs old
70g to 3g as adipose and areolar CT replace
how many lymph nodes/where
along lymphatic vessels 600
lymph node trabeculae
capsular extensions divide the node into compartments, provide support, and provide a route for blood vessels into the interior of a node
outer cortex of lymph nodes
egg-shaped aggregates of B cells called lymphatic nodules
primary lymphatic nodule vs secondary (what is most common in outrer cortex of lymph nodes)
prim: mostly B cells
sec: form in response to an
antigen and are sites of plasma cell (antibody producing) and memory B cell formation
secondary most common
inner cortex of lymph nodes
no lymphatic nodules
consists mainly of T cells and dendritic cells (present antigens to t cells so they proliferate)
lymph node medulla
contains B cells, antibody-producing
plasma cells that have migrated out of the cortex into the medulla, and macrophages
has reticular fibers/cells
lymph flow into/through a lymph node
enters through afferent lymphatic vessels (valves towards)
sinuses (subcapsular->trabecular->medullary)
drain into efferent lymphatic vesels (valves away)
hilum: slight depression where BV join and leave node
how are lymph nodes a filter
lymph enters, reticular fibers trap foreign substances at sinuses
macrophags destroy by phagocytosis
lymphocytes destroy by immune response
largest single mass of lymphatic tissue
spleen
where is spleen
L hypochondriac between stomach and diaphragm
what passes through spleens hilum
splenic artery, splenic vein, efferent L vessels
white pulp (where,consists)
spleen
lymphatic tissue, consisting mostly of lymphocytes and macrophages arranged around branches of splenic artery (central arteries)
red pulp (where, consists)
spleen
consists of blood filled venous sinuses and splenic cords (Billroth’s cords)
white pulp function
B/T cells carry out immune functions
macrophages destroy blood-borne pathogens
red pulp function
(1) removal by macrophages of ruptured, worn out, or defective blood cells and platelets
(2) storage of platelets, up
to one-third of the body’s supply
(3) production of blood cells
(hemopoiesis) during fetal life
mucosaassociated lymphatic tissue (MALT).
AKA lymphatic nodules
called this because scattered throughout the lamina propria (connective tissue) of MM lining the gastrointestinal, urinary, and reproductive tracts and the respiratory airways
where are aggregations of lymphatic nodules
tonsils
Peyer’s patches in ileum of SI
appendix
five tonsils and function
1 pharyngeal: post wall of nasopharynx
2 palatine: post oral cavity, either side
2 lingual: base of tongue
strategically positioned to participate in immune responses against inhaled
or ingested foreign substances
first line of defense (innate)
skin/MM
epidermis
physical barrier, shedding removes microbes, sebum inhibits growth of bacteria/fungi
MM
secete mucus to trap microbes
nose: hairs trap/filter
resp: cilia move stuff towards throat
second line of defense (innate)
internal antimicrobial substances, phagocytes, NK cells, inflammation, fever
gastric juices
mixture of hydrochloric acid, enzymes,
and mucus
acidic: 1.2-3
destroy bacteria
interferons (INFs) (what/function/types)
antimicrobial substance
dont prevent viruses attaching/pentrating but prevent replication with antiviral proteins
3 types: alpha-, beta-,and gamma-IFN
4 types of antimicrobial substances
interferons
complement
iron-binding proteins
antimicrobial proteins
complement system (what/function)
antimicrobial substance
inactive proteins in blood plasma and on PM, when activated they enhance reactions: cytolysis of microbes, promotes phagocytosis, and contributes to inflammation
iron-binding proteins (what. functions, types)
antimicrobial substance
inhibit growth of bactria by reducing iron
transferrin, lactoferrin, ferritin, and hemoglobin
antimicrobial proteins (AMPs)
antimicrobial substance
short peptides
kill a wide range of microbes, attract dendritic cells and mast cells, which participate in immune responses
dont develop resistance
how many lymphocytes in blood are NK cells
5-10 percent
NK cell function/line of defense
2nd
attack any body cells that display abnormal or unusual plasma
membrane proteins
perforin (released by/function)
in granules released by NK cells, cause perforations in cell membrane=inflow of ECF=cytolysis
granzymes
in granule released by NK cells
phagocytes (what/types/function)
NK cells
neutrophils/macrophages
infection=neutrophils/monocytes travel to=monocytes become macrophages, both do phagocytosis
phagocytosis 5 stages
chemotaxis: phagocytes travel to damage
adherence: attachment of phagocyte
ingestion: pseudopods surround MO=phagosome
digestion: phagolysosome; oxidative burst
killing: not degraded materials=residual bodies
phagolysosome
during digestion of phagocytosis whe phagosome enters and merges with lysosome
oxidative burst
during digestion of phagocytosis when phagocyte forms lethal oxidants
inflammation signs/symptoms
PRISH
Pain: due to release of chemicals
redness: blood to area
Immobility: severe case
swelling: accumulation of fluids
heat: blood to area
inflammatory response three stages
(1) vasodilation and increased permeability of blood vessels
(2) emigration (movement) of phagocytes from the blood into interstitial fluid
(3) tissue repair
substances contributing to vasodilation (5)
histamine: vasodilatiom/permeability
kinins: vasodilation/permeability
prostaglandins: intensify histamine/kinins
leukotrienes: permeability/attract phagocytes
complement: complement system
emigration depends on/happens when
chemotaxis
an hour after inflammation starts
leukocytosis
increase in WBC in blood
acute vs chronic inflammation (development, lasting, principal defensive cells)
develop rapidly, last days to weeks, neutrophils vs develop slowly, several months to years, monocytes/macrophages
fever
Intensifies effects of interferons; inhibits growth of some microbes; speeds up body reactions that aid repair
two properties distinguishing adaptive immunity
specificity
memory
two mature t cells that exit thymus
helper T cells AKA CD4 cells
cytotoxic t cells AKA CD8 cells
cell body vs antibody mediated immunity
cytotoxic T cells directly attacking antigens vs B cells -> plasma cells= secrete antibodies
helper t cells help with both
cell mediated immunity effective against
intracellular pathogens (viruses, bacteria, or fungi that are inside cells)
some cancer cells
foreign tissue transplants.
Antibody-mediated immunity effective against
extracellular pathogens (viruses, bacteria, or fungi that are in
body fluids outside cells)
antibody mediated immunity AKA
humoral immunity (as effective against humors/fluids)
clonel selection (what/result/occurs)
process by which a lymphocyte proliferates (divides) and differentiates (forms more highly specialized cells) in response to a specific antigen
result=clone (effector/memory)
occurs in secondary lymphatic organs/tissues
effector cells (what, lifespan, includes)
lymphocyte clones that carry out immune response;most die after immune response
includes:
active helper T cells
active cytotoxic T cells
plasma cells (part of a B cell clone)
memory cells (what, lifespan, includes)
lymphocytes clones that proliferate into effector cells when antibodies enter again; don’t die after immune response
includes:
memory helper T cells
memory cytotoxic T cells
memory b cells
reactivity
ability of the antigen to react specifically with the antibodies or cells it provoked
complete antigens
both immunogenicity/reactivity
immunogenicity
ability to provoke an immune response by stimulating the production of specific antibodies, the proliferation of specific T cells, or both
epitopes (antigenic determinants)
certain small parts of a large antigen molecule acts as the trigger for an immune response
Antigens that get past the innate defenses generally follow one of
three routes into lymphatic tissue
- most that enter bloodstream are trapped in spleen
- penetrate skin=enter lymphatic vessels and lodge in lymph nodes
- penetrate mucous membranes=entrapped by mucosa-associated lymphatic tissue (MALT).
hapten
small particle that has reactivity but not immunogenicity
immune response if attached to larger carrier protein
major histocompatibility complex (MHC) antigens (what/function)
self antigens in PM of all cells except RBC
normal function is to help T cells recognize that an antigen is
foreign, not self
reason for transplant rejecetion
class I vs class II major histocompatibility complex (MHC)
in PM of all cells except RBC vs on antigen-presenting cells
antigen presentation
insertion of MHC into PM
exogenous antigens
foreign antigens that are present in fluids outside body cells
antigen-presenting cells (APCs)
specialized cells that process and present exogenous antigens
dendritic cells, macrophages, and B cells
steps in the processing and presenting of an exogenous antigen by an antigen-presenting cell
- ingestion of antigen
2.digestion of antigen into peptide fragments - synthesis of MHC-II molecules at ER
- packaging of MHC-II molecules into vesicles
- fusion of vesicles
- binding of peptide fragments to MHC-II molecules
- insertion of antigen-MHC-II complexes into PM
processing of endogenous antigens by infected body cell
- Digestion of antigen into peptide fragments
- Synthesis of MHC-I molecules
- Binding of peptide fragments to MHC-I molecules
- Packaging of antigen–MHC-I molecules
- Insertion of antigen–MHC-I complexes into the plasma
membrane
cytokines
small protein hormones that stimulate or inhibit many normal cell functions, such as cell growth and differentiation
T cell receptors (TCRs)
antigen receptors on T cell surface recognize and bind specific antigen fragments of a MHC complex
coreceptors
CD4 or CD8 proteins that interact with the MHC antigens and help maintain the TCR–MHC coupling
costimulation
T cell becomes activated when antigen binds to it and one more signal at the same time
When you insert the correct key (antigen) in the ignition (TCR) and turn it, the car starts (recognition of specific antigen), but it cannot move forward until you move the gear shift into
drive (costimulation).
costimulators
interleukin-2 (IL-2) / other cytokines
pairs of PM molecules one on T cell one on antigen
anergy
state of inactivity when recognition (antigen binding to receptor) without costimulation happens
ex. leaving car in neutral until it runs out of gas
what do active helper t cells (CD4 T cells) start secreting after an hour of costimulation and what is its importance
Interleukin II (IL-2)
needed for virtually all immune responses
prime trigger of T cell proliferation
as a costimulator for resting helper T cells or cytotoxic T cells
enhances activation and proliferation of T cells, B cells, and natural killer cells
positive feedback loop as autocrine or paracrine (costimulator)
T cells displaying CD4 vs CD8
helper T cells vs cytotoxic T cells
cytotoxic cells (CD8 cells) recognize what
foreign antigens combined with MHC-I on the surface of:
1. body cells infected by microbes
2. some tumor cells
3. cells of tissue transplant
what do cytotoxic cells (CD8 cells) need to use as a costimulator
interleukin-2 (IL-2) other cytokines produced by active helper T cells
that have already become bound to copies of the same antigen
cytotoxic T cells vs NK cells
have receptors/kill only one type of microbe vs destroy a wide variety of microbe-infected body cells
cytotoxic T cells using granzymes to kill microbes
using receptors, recognize and
bind to infected target cells that have microbial antigens displayed
on their surface. The cytotoxic T cell then releases granzymes, protein-digesting enzymes that trigger apoptosis Once the infected cell is destroyed, the released microbes are killed by phagocytes.
cytotoxic cells using perforin and granulysin
perforin makes channels into PM=ECF in=cytolysis
granulysin enters channels and destroys microbes
lymphotoxin
toxic molecule released by cytotoxic T cells that activated enzymes in target cell=DNA fragments=death
tumor antigens
normal cell that transforms into cancerous cell displays these components
immunological surveillance
immune responses carried out by cytotoxic T cells, macrophages, and NK cells to remove tumour cells caused by cancerous causing viruses
immunosuppressive drugs to prevent transplant rejection cause an increased chance in
virus-associated cancers (other cancer types aren’t increased)
B cells stay put in
a lymph node, the spleen, or mucosa-associated lymphatic tissue
can B cells respond to an unprocessed antigen present in lymph or interstitial fluid
yes but their response is much more intense when they process the antigen
antigen in a B cell processing occurs
antigen into B cell, broken down into peptide fragments, combined with MHC-II self-antigens, and moved to B cell PM
Helper T cells recognize the antigen–MHC-II complex and produce interleukin-2 and other cytokines that function as costimulators to activate B cells
A few days after exposure to an antigen, a ____ _____ secretes hundreds of millions of antibodies each day for about ___ or ___ days, until the plasma cell dies
plasma cell
4
5
antibodys AKA
immynoglobulins (Igs)
antibody structure
2 heavy chains: 450 AA+short carbohydrate chain attached to each heavy
2 light chains: 220 AA
disulfide bond (S-S) holds light to heavy and midregion to heavy
hinge region: T or Y shape
stem region: beyond hinge region
epitope
part of antigen that connects with antibody
antibody actions
neutralizing antigen
immobilizing bacteria
agglutinating and precipitating antigen (clump together)
activating complement
enhancing phagocytosis
IgG (percentage, found, size, protection, special)
80 percent of AB in blood
found in blood lymph intestines
monomer
Protects against bacteria and viruses by enhancing phagocytosis, neutralizing toxins, and triggering complement system
can cross placenta
classes of immunoglobulins
IgG, IgA, IgM, IgD, IgE
IgM (percentage, found, size, protection, special)
5-10
blood/lymph
pentamers (5), monomers on B cells
1st antibody secreted, activates complement and causes agglutination and lysis of microbes
anti-A/B antibodies of ABO blood group are IgM
IgA (percentage, found, size, protection, special)
10-15
mainly sweat, tears, saliva, mucus, breast milk, and GI secretions some in blood/lymph
monomers and dimers
Provides localized protection of MM
against bacteria and viruses
levels decrease during stress=less resistance
IgD (percentage, found, size, protection)
0.2
surfaces of B cells as antigen receptors
monomers
involved in activation of B cells
IgE (percentage, found, size, protection, special)
less than 0.1
on mast cells and basophils
monomers
Involved in
allergic and hypersensitivity reactions; protects against parasitic worms
complement system
defensive system made up of over 30 proteins produced by the liver and found circulating in blood plasma and within tissues throughout the body
destroy microbes by causing phagocytosis, cytolysis, and inflammation; they also prevent excessive damage to
body tissues
complement cascade of reactions
- inactivated Cs splits to activated C3a/C3b
- C3b binds to microbe/phagocytes attach to C3b=enhances phagocytosis by opsonization (coating a microbe)
- C3b splits C5, C5b binds to C6/C7 and attach to PM of microbe, C8 and C9 join the other complement proteins and together form a cylinder-shaped membrane attack complex, which inserts into the plasma membrane
- membrane attack complex makes channels=cytolysis
- C3a/C5a bind to mast cells=histamine release=inflammation, C5a attracts phagocytes to inflammation (chemotaxis)
C3 activated 3 ways
classical pathway: antibodies bind to antigens=activates C1=C3 activates=phagocytosis, cytolysis, inflammation
alternative pathway: initiated by an interaction between lipid–carbohydrate complexes on the surface of microbes and complement protein factors
B, D, and P (no antibodies)
lectin pathway: macrophages that digest microbes release chemicals that cause the liver to produce proteins called lectins. Lectins bind to the carbohydrates on the surface of microbes=C3 activation
immunological memory
due to the presence of long-lasting antibodies and very long-lived lymphocytes that arise during clonal selection of antigen-stimulated B cells and T cells
primary vs secondary response
prim: After an initial contact with an antigen, no antibodies are present for a period of several days. Then, a slow rise in the antibody titer occurs, first IgM and then IgG, followed by a gradual decline in antibody titer
sec: After subsequent encounters, the antibody titer is far greater than during a primary response and consists mainly of IgG antibodies
naturally acquired active immunity
Following exposure to a microbe, antigen recognition by B cells and T cells and costimulation lead to formation of antibodysecreting plasma cells, cytotoxic T cells, and B and T memory cells
Naturally acquired passive immunity
IgG antibodies are transferred from mother to fetus across placenta, or IgA antibodies are transferred from mother to baby in milk during breast-feeding
artificially aquired active immunity
Antigens introduced during vaccination stimulate cell-mediated and antibody-mediated immune responses, leading to production of memory cells. Antigens are pretreated to be immunogenic but not pathogenic (they will trigger an immune response but not cause significant illness)
artificially acquired passive immunity
intravenous injection of Igs (antibodies)
T cells two traits
self-recognition: recognize your own major histocompatibility complex (MHC) proteins
self-tolerance: lack reactivity to peptide fragments from your own proteins
positive selection
Pre-T cells in the thymus develop the capability for self-recognition
some pre-T cells express T-cell receptors (TCRs) that interact with self MHC proteins on epithelial cells in the thymic cortex
negative selection
development of self-tolerance occurs by a weeding-out process in which t cells interact with dendritic cells at junction of cortex and medulla in thymus
deletion: self-reactive undergo apoptosis
anergy: remain alive but unresponsive to antigenic stimulation
how many immature T cells survive positive and negative selection
1-5 percent
B cells develop self-tolerance by
undergoing deletion in bone marrow and anergy when released into blood
antigen presenting cells
macrophages
dendritic cell
b cell
macrophage review
Processing and presentation of foreign antigens to T cells
secretion of interleukin-1, which stimulates secretion of interleukin-2
by helper T cells and induces proliferation of B cells
secretion of interferons that stimulate T cell growth
dendritic cell review
Processes and presents antigen to T cells and B cells; found in mucous membranes, skin, lymph nodes
B cell review (as antigen-presenting cell)
Processes and presents antigen to helper T cells
cytotoxic t cell review
Kills host target cells by releasing granzymes that induce apoptosis, perforin that forms channels to cause cytolysis, granulysin that destroys microbes, lymphotoxin that destroys target cell DNA, gamma-interferon that attracts macrophages and increases
their phagocytic activity, and macrophage migration inhibition factor that prevents macrophage migration from site of infection
helper t cell review
Cooperates with B cells to amplify antibody production by plasma cells and secretes interleukin-2, which stimulates proliferation of T cells and B cells
May secrete gamma-IFN and tumor necrosis factor (TNF), which stimulate inflammatory response
memory t cell review
Remains in lymphatic tissue and recognizes original invading antigens, even years after first encounter
b cell review (as lymphocyte)
Differentiates into antibody-producing plasma cell
plasma cell review
Descendant of B cell that produces and secretes antibodies
memory b cell review
Descendant of B cell that remains after immune response and is ready to respond rapidly and forcefully should the same antigen enter body in future
