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242 Cards in this Set

  • Front
  • Back
ability to ward off disease caused by microbes or their products and to protect against environmental agents
Immunity or Resistance
vulnerability or lack of immunity
- defenses present at birth
- always present
- rapid response for disease prevention
- no specificity
- no memory component
- first and second lines of defense
- prevention of microbe access to body and elmination of those that gain access
Innate (nonspecific) immunity
- defenses that involve specific recognition of microbe one it has breached first/second lines of defense
- based on specific response to specific microbe
- adapts/adjusts to handle particular microbe
- slower to respond
- involves lymphocytes (T and B cells)
Adaptive (specific) immunity
- innate system responses are activated by these protein receptors in the plasma membrane of defensive cells
- attach to components of microbes
- induce defensive cells to release chemicals called cytokines
Toll-like receptors (TLRs)
proteins that regulate the intensity of and duration of immune responses
- one role is to recruit other macrophages and dentritic cells as well as othe defensive cells to isolate and destroy the microbes as part of the inflammatory response
- also activate T and B cells involved in adaptive immunity
skin and mucous membranes
first line of defense
- barriers to entry or processes that remove microbes from the body's surface
physical factors of innate immunity
substances made by the body that inhibit microbial growth or destroy them
chemical factors of innate immunity
one of the largest organs of the human body based on surface area
skin's inner, thicker portion, composed of connective tissue
outer, thinner portion of the skin, in direct contact with the environment
consists of many layers of continous sheets of tightly packed epithelial cells
protective protein in the top layer of dead epidermal cells
factors that inhibit microbe growth on the skin
- top layer of skin shed periodically
- dryness of skin
what areas of skin are microbes most present
moist areas of skin
bacteria most likely to cause a skin infection
where are staphylococci found on the skin
epidermis, hair follicles, sweat and oil glands
what can infections of the skin be due to?
burns, cuts, stab wounds, or other conditions that break the skin
cells that line blood and lympathic vessels that are not as closely packed as epidermal cells
epithelial cells
consist of an epithelial layer and underlying connective tissue layer
inhibit entrance of many microbes, but offer less protection than the skin
mucous membrane
what do the mucous membranes line?
GI, respiratory, genitourinary tracts
- secreted by the epithelial layer of a mucous membrane
- slightly viscous glycoprotein produced by goblet cells of a mucous membrane
functions of mucus
prevents tracts from dryhing out
pathogen that can penetrate the mucous membrane if present in sufficient numbers
Treponema pallidum
group of structures that manufactures and drains away tears
lacrimal apparatus
located toward the upper, outermost portion of each eye socket
produce tears and pass them under the upper eyelid
lacrimal glands
how does the lacrimal apparatus help prevent microbial growth?
continual washing action of the eye
produced by the salivary glands
helps dilute numbres of microbes and wash them from surface of the teeth and mucous membranes of the mouth
how does mucus help defend the respiratory and GI tracts?
it traps many of the organisms that enter
what structures in the nose also help filter inhaled air and trap microorganisms, dust, and pollutants?
mucus-coated hairs
these cover the cells of the mucous membrane of the lower respiratory tract
move synchronously
synchronous movement of cilia to move mucus toward the throat
ciliary escalator
also prevents microbes from entering the lower respiratory tract, small lid of cartilage covering larynx during swallowing
this cleanses the urethra
this cleans out the vagina
vaginal secretions
these expel microbes forcefully, such as in response to microbial toxins
defecation and vomiting
produced by sebaceous (oil) glands
prevents hair from drying
forms protective film over the surface of the skin
contains unsaturated fatty acids (low pH)
what is body odor caused by?
commensal bacteria that live on the skin and decompose sloughed off skin cells and the end products of that metabolism
what causes inflammation that is associated with acne?
certain bacteria that metabolize debum, which forms fatty acids that cause the inflammation
produced by sweat glands
helps maintain body temp, eliminate some wastes, flush microbes from the surface of the skin
enzyme capable of breaking down cell walls of gram (+) bacteria and to lesser extent gram (-) bacteria.
what does lysozyme specifically break down?
chemical bonds on the peptidoglycan
what is lysozyme found in?
tears, saliva, nasal secretions, tissue fluids
produced by the glands of the stomach
mixture of HCl, enzymes, mucus
gastric juice
what is the pH of gastric juice?
1.2 - 3.0
What bacteria can gastric juice not kill?
Clostridium botulinum and Staphylococcus aureus
How can some bacteria survive the stomach?
protection by food particles
Which bacterium neutralizes stomach acid and allows growth and what does it cause?
Helicobacter pylori

Ulcers and gastritis
How does normal flora prevent overgrowth of pathogens?
- competitive exclusion
- producing substances harmful to pathogens
- altering conditions like pH and oxygen availability
What normal flora bacteria are opportunistic pathogens?
E. coli, S. aureus, S. epidermis, Enterococcus faecalis, Pseudomonas aeruginosa, oral streptococci.
What does the second line of defense consist of?
phagocytic cells, inflammation, fever, antimicrobial substances
fluid that blood consists of
what are formed elements?
cells and cell fragments
another name for white blood cells
increase in number of WBC's in response to combat microbes
diseases that might cause elevation in leukocyte count
meningitis, infectious mononucleosis, appendicitis, pneumococcal pneumonia, gonorrhea
what is a decrease in the leukocyte count?
what diseases may cause a decrease in leukocyte count?
salmonella, brucellosis, viral and rickettsial infections
what factors may cause leukopenia?
- impaired white blood cell production
- increased sensitivity of WBC membranes to damage by complement
how can leukocyte increase be detected?
differential white blood cell count which is calculation of % of each kind of WBC in sample of 100
what are the two main categories of leukocytes?
granulocytes, agranulocytes
What distinguish the granulocytes?
large granules in their cytoplasm visible with staining
What are the different types of granulocytes?
neutrophils, basophils, eosinophils, dendritic cells
stain pale lilac with mixture of acidic and basic dyes
also known as polymorphonuclear leukocytes (PMN's)
highly phagocytic and motile
active in the inital stages of an infection
have ability to leave blood, enter infected tissue, and destroy microbes/foreign particles
stain blue-purple with methlyene blue
release substances like histamine that are important in inflammation and allergic responses
stain red or orange with dye eosin
somewhat phagocutic and have ability to leave blood
major fxn: to promote toxic proteins against parasites by attaching to outer surface and discharging peroxide ions to kill them
long extensions
abundant in epidermis of skin, mucous membranes, thymus, lymph nodes
fxn: destroy microbes by phagocytosis and to initiate adaptive immunity responses
dendritic cells
have granules in cytoplasm but not visible under microscope after staining
Name the different types of agranulocytes
monocytes, lymphocytes (NK cells), T cells, B cells
not actively phagocytic until they leave blood, enter tissues, and mature
mature monocyte
one factor responsible for swelling of lymph nodes during an infection
maturation and proliferation of macrophages (as well as lymphocytes)
what do macrophages do?
- remove microbes that pass through organs that contain them by phagocytosis
- dispose of worn out blood cells
what types of cells are classified as lymphocytes?
natural killer cells
T cells
B cells
Where are natural killer cells found?
blood and spleen
lymph nodes
red bone marrow
What do NK cells target?
infected body cells and certain tumor cells
cells that display abnormal or unusual plasma membrane proteins
How do NK cells kill other cells?
- binding causes release of granules that contain toxic substances
What are perforins and what do they do?
protein that inserts into plasma membrane of target cell and creates channels in the membrane, causing extracellular fluid to rush in and burst the cell
what is cytolysis?
bursting of a cell due to extracellular fluid rushing in
What are granzymes?
protein-digesting enzymes that induce the target cell to undergo apoptosis (self-destruction)
What do granzymes kills?
infected cells, but not microbes inside those cells
Where are T and B cells found?
lymphoid tissues of the lymphatic system: tonsils, spleen, thymus, thoracic duct, red bone marrow, appendix, Peyer's patches of small intenstine, lymph nodes in the resp, GI, and reprod tracts
also circulate in the blood
ingestion of a microbe or particle by a cell
what types of cells are phagocytes?
WBCs or derivatives of them
What are some of the activators of phagocytes?
components of bacteria (lipid A or LPS)
small protein hormones called cytokines, secreted by phagocytes and other cells involved in adaptive immunity
what cells migrate to an infection?
granulocytes (esp. monocytes) and monocytes
what happens to monocytes during the migration to an infection?
they enlarge and develop into actively phagocytic macrophages
they leave the blood and migrate into tissues where they develop into macrophages
what are fixed macrophages?
macrophages located in tissues and organs
what are wandering macrophages?
roam tissues and gather and sites of infection or inflammation
what do the various macrophages constitute?
the mononuclear phagocytic (reticuloendothelial) system
During the course of an infection, which blood cells dominate?
- initial phase: granulocytes, esp. neutrophils, actively phagocytic
- as progresses: macrophages dominate, scavenge and phagocytize remaining living bacteria and dead/dying bacteria
- viral/fungal infections: macrophages dominate all phases
what are the four main phases of phagocytosis?
- chemotaxis
- adherence
- ingestion
- digestion
What is chemotaxis and name some chemicals involved
- the chemical attraction of phagocytes to microbes
- chemicals that attract phagocytes: microbial products, components of WBCs, damaged tissue cells, peptides derived from complement
What is adherence and how does it work?
- attachment of the phagocyte's plasma membrane to the surface of microbe or other foreign material
What is opsonization?
coating of microorganism to make it more easily phagocytized
the coating is made of serum proteins that promote attachment of the microbe to the phagocyte
what are opsonins?
the proteins involved in opsonization
What happens during ingestion?
plasma membrane of phagocyte extends psuedopods that engulf the organism
psuedopods meet and form a phagosome.
membrane pumps protons into the phagosome, reducing pH, activating hydrolytic enzymes
what happens in the digestion phase of phagocytosis?
fusion of phagosome with lysosome to form phagolysosome
digestion of ingested microbe by enzymes
formation of residual body containing indigestible material
discharge of waste materials
what is the structure called that results from the merging of a lysosome and a phagosome?
what is in a lysosome?
lysozyme - affects the peptide cross-links
other enzymes in it too, like lipase, proteases, ribonucleases, etc.
enzymes that produce toxic oxygen products
What is the process by which toxic oxygen products are produced?
oxidative burst
what is the indigestible material inside of a phagolysosome called?
residual body
what are the six methods of avoiding destruction by phagocytes?
M protein
membrane attach complexes
prevention of phagolysosome formation
What are M proteins? What is an example of bacteria that use them?
inhibits the attachment of phagocytes to their surfaces and makes adherence more difficult

Strep pyogenes
How do capules help avoid destruction by phagocytes? What bacteria use them?
- allows bacterium to slide away
- Strep pneumoniae, Haemophilus influenza type B
What are leukocidins?
they cause release of the phagocyte's own lysosomal enzymes into its cytoplasm.

Staph genus
What are membrane attack complexes?
lyse phagocyte cell membranes once inside phagocyte and then release the bacteria so they can replicate in the cytoplasm
they then release more, which lyses the cell and allows infection of other cells by bacteria.
what damage triggers inflammation?
microbial infection
physical agents
chemical agents
what are the four signs and symptoms of inflammation? what is the fifth?
- redness
- pain
- heat
- swelling
- loss of function
what is acute inflammation?
- where cause of inflammation removed in short period of time
what is chronic inflammation?
- cause is more difficult to remove
- reponse longer lasting but less intense
what are the functions of inflammation?
- destroy the injurious agent, remove it and its by products from body
- limit effects on the body by confining it and byproducts
- repair or replace damaged tissued
what are acute-phase proteins?
- they are activated and conc. is increased during inflammation
- come from liver/blood
- localized and systemic responses: complement, cytokines, specialized proteins (fibrinogen, kinins)
what are the three phases of inflammation?
- vasodilation and increased permeability of blood vessels
- phagocyte migration and phagocytosis
- tissue repair
what is vasodilation?
increased blood flow to the damaged area and is responsible for redness and heat assoc. with inflammation
what does vasodilation do?
increase diameter of blood vessels
increase permeability
how does increased permeability help?
- permits defensive substances normally in blood to pass through walls of the blood vessels and enter the injured area
what is edema?
what is the pain of inflammation caused by?
nerve damage
pressure of edema
what chemicals are involved in vasodilation and the increase of permeability?
- histamine
- kinins
- prostoglandins
- leukotrienes
where is histimine found?
- mast cells in connective tissue, basophils, blood platelets
when is histimine released?
in direct response to the injury of cells that contain it
also released in response to stimulation by certain components of the complement system
what are kinins and where are they found?
- found in blood plasma
- cause vasodilation and increased perm of blood vessels
- attract pagocytic granulocytes (neutrophils mostly) to injured areas
what are prostoglandins?
substances released by damaged cells
intensity effects of histimine, kinins and help phagocytes move through cell walls
what are leukotrienes?
produced by mast cells and basophils
cause increased perm of blood vessels and help attach phagocytes to pathogens
what are mast cells?
they are in connective tissue of skin and resp system and in blood vessels
what is the purpose of a blood clot?
prevent microbe or toxins from spreading
what is pus?
mixture of dead cells and body fluids in a navity formed by the breakdown of body tissues
what is a focus of infection called?
how soon after inflammation is intiated does phagocyte migration start?
within one hour
what happens in phagocyte migration and phagocytosis?
- margination
- emigration (diapedesis)
- phagocytosis
what is margination?
sticking of neutrophils and monocytes to the inner lining of blood vessels as blood flow decreases
what is emigration?
when phagocytes squeeze between endothelial cells to reach the damaged area, can take as little as 2 minutes
what are chemokines?
cytokines that are chemotactic for phagocytes and T cells and stimulate both the inflammatory response and an adaptive immune response
where does the flow of neutrophils come from during inflammation?
prouctiona nd relase of additional granulocytes from red bone marrow
which of these two go to the infected area first? (monocytes or granulocytes)
what happens to monocytes in the infected area?
they undergo changes in biological properties and become wandering macrophages
compare macrophages to granulocytes
granulocytes: predominate early in an infection
die off rapidly
macrophages: more phagocytic
large enough to phagocytize destroyed tissue, granulocytes that have been destroyed, and invading microbes
why does pus form?
dying granulocytes or macrophages
may push to the surface of body or into internal cavity for removal
what conditions may phagocytosis not work well?
- organ transplant-related drugs to suppress rejection
- individ. born with inability to produce them
- radiation treatments -> damaging red bone marrow
- AIDS/cancer
when does tissue repair begin?
during active phase of inflammation but cannot be completed until all harmful substances have been removed/neutralized at site of injury
name tissue that can regenerate/repair itself well and one that cannot
well: skin
not well: cardiac muscle
when is a tissue repaired?
when its stroma or parenchyma produces new cells
what is the stroma?
supporting connective tissue (capsule around liver)
what is the parenchyma?
the functioning part of the tissue (liver cells)
when is scar tissue formed?
when repair cells of stroma more active
more perfect when only parenchymal cells active
what is fever?
abnormally high body temperatuer
what is the most freq cause of fever?
infection from bacteria (and their toxins) or viruses
what part of the brain controls body temperature?
name two substances that can affect the hypothalamus by setting it at a higher temperature
- cytokine interleukin-1 - released by phagocytes when they ingest gram (-) bacteria
- cytokine alpha-tumor necrosis factor (produced by macrophages and mast cells)
when thermostat is set higher, how does the body respond?
- blood vessel constriction
- increased rate of metabolism
- shivering
what is a chill?
skin remains cold, shivering
sign that body temp. is rising
disappears when body temp reached
when does fever go down?
when IL-1 eliminated
what is crisis?
when body temp is going down
vasodilation and sweating
how does fever act as a defense against disease?
- IL-1 steps up prod. of T-cells
- intensifies effect of antiviral interferons
- increases prod. of transferrins that decrease available iron for microbes
- speeds up body's reactions: help body tissues repair more quickly
complications of fever
- tachycardia (rapid heart rate)
- increased metabolic rate
- dehydration
- electrolyte imbalances
- coma
- fever above 112-114F -> death
what is the complement system?
- defensive system consisting of over 30 proteins produced by the liver and found circulating in blood serum and within tissues throughout the body
how does the complement system destroy microbes?
- cytolysis
- inflammation
- phagocytosis
how are complement proteins designated?
proteins C1-C9
fragments a, b
what are activated fragments?
they carry out destructive actions of C1-C9 complement proteins
how do complement proteins act?
in a cascade
why is activation of C3 important?
starts a cascade that results in cytolysis, inflammation, and phagocytosis
how do host cells avoid lysis?
they contain proteins that protect against lysis by preventing attachment of MAC proteins to their surfaces
what pathways initiate the complement cascade?
- classical pathway
- alternative pathway
- lectin pathway
how is the classical pathway initiated?
when antibodies bind to antigens on microbes
how is the alternative pathway initiated?
by contact between complement proteins (B, D, P) and lipid-carb on the surface of the antigen and C3.
how is the lectin pathway initiated?
macrophages digesting foreign matter release chemicals that stimulate the liver to produce lectin. mannose-binding lectin binds to carb mannose in bacterial cell walls and on some viruses.
recognize specific pattern of carbs
actgs as opsonin
how is complement inactivated?
by regulatory proteins in the host's blood and on certain cells
what does serum resistant mean?
bacteria that are not killed by the MAC
what are interferons?
antiviral proteins produced by lymphocytes and macrophages after viral stimulation
interfere with viral replication
describe the specificity of interferons
specific for a host cell and not a specific virus, active against a number of viruses
name the three types of human interferons
describe alpha-interferon and beta-interferon
produced by virus-infected host cells in small quantities and diffuse to uninfected neighboring cells
react with plasma or nuclear membrane receptors, inducing production of AVP (anti-virus proteins)
describe gamma-interferon
produced by lymphocytes
induces neutrophils and macrophages to kill bacteria by phagocytosis
what are the problems with interferons?
- short-lived, not stable for long periods of time
- side effects when injected
- high concentrations are toxic- - no effect on already-infected cells
- some viruses are resistant
- some viruses do not induce enough production of AVPs
why are recombinant interferons important?
- plentiful
- pure
what are transferrins?
iron-binding proteins in blood, milk, teras, saliva
inhibit bacterial growth by reducing amt of available iron
what are antimicrobial peptides?
peptides (~12 amino acids) bind to microbial plasma membranes causing cell lysis
produced by mucous membrane cells and phagocytes
what is the difference between innate and adaptive immunity?
- innate: defenses always present
- adaptive: adapts to specific invader or foreign substance
what is vaccination?
exposing people to harmless versions of pathogens that caused certain diseases rendering them immune
what does antigen stand for?
antibody generator
where are antibodies found?
in the blood serum
what happens when antibodies and antigens combine?
they clump together
what is humoral immunity?
immunity brought about by antibodies
what is needed for maturation of immune system?
- bursa (thymus)
what is the source of lymphocytes in the first few weeks of development? after that?
red bone marrow
what are lymphocytes that mature in the bone marrow?
b cells
how do b cells recognize different antigens?
by antibodies/immunoglobulins that coat their surface with receptors to the antigens
what are other lymphocytes that do not have surface immunoglobulins but mature under influence of thymus?
T cells (basis of immunity)
where are T and B cells primariliy found?
blood and lymphoid organs
how do T cells respond to antigens?
receptors on surface called T-cell receptors
what does contact w/ an antigen complementary to a TCR do?
causes certain types of T cells to proliferate and secerete cytokines rather than antibodies
what are cytokines?
chemical messengers that impart instructions to other cells to perform certain functions
what do antigens dO?
provoke specific immune response that results in production of antibodies that are capable of recognizing the antigen that gave rise to them
whath are antigens that cause a specific immune response called?
what are antigens composed of?
proteins, large polysaccarides
components of invading microbes or surface molecules of other things
what specific regions on antigens to antibodies interact with?
epitope, antigenic determinants
what are haptens?
low molecular weight compounds that are too small to stim. antibody formation alone. but when compiled with carrier molecule, usually serum protein, it and its carrier together form a conjugate that can stimulate an immune response
what does Ig stand for?
what are antigen-binding sites?
2+ identical sites that antibodies bind to
what is the valence?
number of antigen-binding sites on an antibody
what protein chains does a antibody have?
two light chains
two heavy chains
joined by disulfide links and other bonds, form Y shaped molecule
what sections are the variable regions?
seconds at the ends of the Y's arms
bind to the epitopes
what are the constant regions?
the stem and lower parts
what is the stem called?
Fc region (fragment that crystallized)
what can the Fc region do?
- can bind complement
- may bind to cell
which antibodies cross the placental barrier?
which antibodies compose 80% of all antibodies in serum?
how much of the serum antibodies does IgM make up?
what is the predominant type of antibody involved in response to ABO blood group
which antibodies respond to a primary infection and is relatively short-lived?
which antibodies are long-lived?
where is IgA found?
mucous membanes, saliva, milk, etc.
what is the most abundant immunoglobulin in the body?
what is a secretory component?
part of the IgA dimer that protects it from enzymatic degradation
what is the main function of secretory IgA?
prevent the attachment of microbial pathogens to mucosal surfaces, important in respiratory infections
what do we know about IgD antibodies?
looks like igG
found in blood, lymph, on surface of B cells
what are IgE
on mast cells and basophils (participate in allergic reactions)
antigen like pollen links with IgE antibodies, histamine is released
when is the concentration of IgE highest?
parasitic infections, allergic reactions
which cells produce antibodies?
lymphocytes called B cells
what are the majority of B cell surface immunoglobulins?
when is a b cell activated?
when B cells immunoglobulins bind to the epitote for which it is specific
what does an activated B cell undergo?
clonal expansion
what is an antigen that requires a helper T cell for antibody production called?
T-dependent antigen
what happens when a B cell contacts an antigen?
antigen fragments and MHC are combined and displayed on the B cell surface for identification by the TCRs (t-cell receptors)
what is MHC?
molecule that identifies the host and prevents immune system from making antibodies that would be harmful to the host
what MHC is found only on the surface of antigen-presenting cells?
MHC class II
what do cytokines do?
deliver a message from the helper T cells that causes activation of the B cell, which proliferates into many cells
what are the many types of cells that may result from the proliferation of a B cell?
plasma cells (produce antibodies)
memory cells (responsible for enhanced 2ndary response to an antigen)
what is this proliferation of cells called?
clonal selection
how are b cells that are harmfully reactive against self eliminated?
clonal deletion, during immature lymphocytic phase
what are antigens that stimulate b cells without help of t cells?
t-independent antigens
what is a characteristic of these t-independent antigens?
have repeating subunits
can bind to multiple b cell receptors
are memory cells produced with t-independent antigens? what is the response typically?
IgM antibodies
about how many antigens might be recognized by a body?
when does an antigen-antibody complex form?
when antibody encounters antigen for which it is specific
what is the strength of the antigen-antibody complex called?
how is the binding of antibody to antigen useful to the host?
tags foreign cells and moelcules for destruction by phagocytes and complement
what is agglutination?
when antibodies bind to different foreign cells. IgG can do two, but IgM can bind to a lot more
compare and contrast opsonization and antibody-dependent cytokine-mediated cytotoxicity
- both: target organism gets coated with antibodies
- opsonization: destruction by phagocytes
- adcmc: cell destroyed by immune cell external to it
what is neutralization?
IgG antibodies inactivate viruses by blocking their attachment to host cells
what antibodies may trigger activation of the complement system?
IgG, IgM