Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
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
|
Susceptibility
|
|
|
- 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 |
cytokines
|
|
|
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
|
|
|
skin's inner, thicker portion, composed of connective tissue
|
dermis
|
|
|
outer, thinner portion of the skin, in direct contact with the environment
consists of many layers of continous sheets of tightly packed epithelial cells |
epidermis
|
|
|
protective protein in the top layer of dead epidermal cells
|
keratin
|
|
|
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
|
staphylococcus
|
|
|
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 |
mucus
|
|
|
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 |
saliva
|
|
|
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 |
cilia
|
|
|
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
|
epiglottis
|
|
|
this cleanses the urethra
|
urine
|
|
|
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) |
sebum
|
|
|
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 |
persperation
|
|
|
enzyme capable of breaking down cell walls of gram (+) bacteria and to lesser extent gram (-) bacteria.
|
lysozyme
|
|
|
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
|
plasma
|
|
|
what are formed elements?
|
cells and cell fragments
|
|
|
another name for white blood cells
|
leukocytes
|
|
|
increase in number of WBC's in response to combat microbes
|
leukocytosis
|
|
|
diseases that might cause elevation in leukocyte count
|
meningitis, infectious mononucleosis, appendicitis, pneumococcal pneumonia, gonorrhea
|
|
|
what is a decrease in the leukocyte count?
|
leukopenia
|
|
|
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 |
neutrophils
|
|
|
stain blue-purple with methlyene blue
release substances like histamine that are important in inflammation and allergic responses |
basophils
|
|
|
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 |
eosinophils
|
|
|
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
|
agranulocytes
|
|
|
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
|
monocytes
|
|
|
mature monocyte
|
macrophage
|
|
|
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
|
phagocytosis
|
|
|
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?
|
phagolysosome
|
|
|
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
capsules leukocidins 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?
|
swelling
|
|
|
what is the pain of inflammation caused by?
|
nerve damage
toxins 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?
|
abcess
|
|
|
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)
|
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?
|
hypothalamus
|
|
|
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?
|
C
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
|
alpha-interferon
beta-interferon gamma-interferon |
|
|
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?
|
liver
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?
|
immunogens
|
|
|
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?
|
immunoglobulin
|
|
|
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?
|
IgG
|
|
|
which antibodies compose 80% of all antibodies in serum?
|
IgG
|
|
|
how much of the serum antibodies does IgM make up?
|
5-10%
|
|
|
what is the predominant type of antibody involved in response to ABO blood group
|
iGM
|
|
|
which antibodies respond to a primary infection and is relatively short-lived?
|
IgM
|
|
|
which antibodies are long-lived?
|
IgG
|
|
|
where is IgA found?
|
mucous membanes, saliva, milk, etc.
|
|
|
what is the most abundant immunoglobulin in the body?
|
IgA
|
|
|
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?
|
IgM IgD
|
|
|
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?
|
no
IgM antibodies |
|
|
about how many antigens might be recognized by a body?
|
10^15
|
|
|
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?
|
affinity
|
|
|
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
|
