Term
|
Definition
- structures, chemicals, and processes that work together to prevent entry of pathogen
- barriers
-when pierced, broken, or damaged they become portals of entry
* skin, mucous membranes are the first and best defenses.
* mucous membranes are easier to enter than skin because skin has layered,tightly packed cells with a dead layer.
* Lysozymes are present on skin as well
*defacation, urination, peristalsis, blood flow, microbiota, vomitting are all forms of first line of defense also
FIRST LINE IS NON SPECIFIC AND INNATE |
|
|
Term
| is the first line of defense specific or nonspecific |
|
Definition
|
|
Term
| which defense is urine, vomitting, defacation, blood flow, peristalsis, microbiota??? |
|
Definition
|
|
Term
| staphylococcus aureus has what that compromises the first line of defense? |
|
Definition
|
|
Term
|
Definition
1. cells (phagocytes and leukocytes esp)
2. antimicrobial chemicals (complement, interferons)
3. processes (inflammation, fever)
4. contained in or originate in blood
INNATE, NONSPECIFIC |
|
|
Term
| is the second line of defense nonspecific or specific ? |
|
Definition
|
|
Term
| what two general cell types are most important in the second line of defense? |
|
Definition
|
|
Term
| complement, interferon, and other antimicrobial chemicals are an example of which line of defense? |
|
Definition
|
|
Term
| what are the 5 WBC cells of defense |
|
Definition
1. basophils- inflammatory chemicals released
2. eosinophils- worms, allergies (some phago but not imp)
3. neutrophils- phagocytosis
4. lymphocytes- adaptive immunity (involves 3rd line)
5. monocytes- phagocytosis (become macrophage when mature) |
|
|
Term
| a monocyte becomes what when mature |
|
Definition
|
|
Term
| which of the 5 WBCs are involved with adaptive immunity or the 3rd line of defense? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| which WBC helps defend against worms and allergies |
|
Definition
|
|
Term
| which WBC helps promote inflammation? |
|
Definition
|
|
Term
| what 4 WBC types are involved in innate immunity? |
|
Definition
1. eosinophil- allergies, worms
2. basophil- inflammation
3. monocyte- phagocytosis
4. neutrophil - phagocytosis |
|
|
Term
| what two WBC are important in phagocytosis? |
|
Definition
| monocytes (macrophages when mature) and neutrophils |
|
|
Term
|
Definition
| you are born with it and it is fully functional at birth |
|
|
Term
| what is released during inflammation |
|
Definition
| prostaglandins, leukotrenes, histamine |
|
|
Term
| what are the three functions of inflammation |
|
Definition
1. vaso dilation resulting in increased blood flow and permeability of vessels (molecules may now leave blood and enter tissue)
2. migration of leukocytes (macrophage and neutrophils) to site
3. tissue repair (phagocytosis occurs) |
|
|
Term
| what are the two types of inflammation |
|
Definition
1. acute- tissue damage, chemicals released, beneficial
2. chronic- very damaging (ex: arthritis) |
|
|
Term
| arthritis is an example of ________ inflammation |
|
Definition
|
|
Term
| acute inflammation is ____________ to us |
|
Definition
|
|
Term
| what are the 6 steps of Phagocytosis |
|
Definition
1. phagocyte chemotaxis- movement of phagocytes towards chemicals released due to tissue damage
2. phagocyte adherence- must physically bind to bacteria/pathogen
3. ingestion of target- endocytosis takes place, at end pathogen is inside a PHAGOSOME
4. fusion of lysosome to phagosome (also called maturation)
5. killing of target due to digestive enzymes from lysosome
6. elimination of debris |
|
|
Term
|
Definition
| when a phagocyte ingests a pathogen, the pathogen is taken into the cell and a PHAGOSOME is created where it is stored |
|
|
Term
| when phagocytosis takes place digestive enzymes from _________ are responsible for actually killing the pathogen |
|
Definition
|
|
Term
| a _____________ fuses to a phagosome during the 4th stage go phagocytosis |
|
Definition
|
|
Term
| what are some examples of anti-phagocytic factors that pathogens may posses |
|
Definition
1. capsule (prevents attachment)
2. Leukocydins (kills WBC) |
|
|
Term
| what are some nonspecific chemicals involved in the second line of defense? |
|
Definition
| interferon and complement |
|
|
Term
|
Definition
Interferon- protein molecules released by host cells to nonspecifically inhibit the spread of viral infections
*they interfere with viral replication in NEIGHBORING cells
* the infected cell produces a protein that turns on expression of antiviral protein in neighboring cells
STEPS
1. cell virally infected, interferon made
2. shoots out interferon to neighbors, the cell is dead already when virally infected, but it helps out neighbors not infected yet. |
|
|
Term
interferon is made by who?
to protect who? |
|
Definition
virally infected cells
protects neighboring cells |
|
|
Term
|
Definition
complement- set of blood proteins which initially act as opsonins (assist in phagocytosis) and chemotactic factors that indirectly trigger inflammation and fever.
- 9 proteins
-always present in blood, but in an inactive state
- activation occurs by binding of C1 to fragment crystallizable (Fc) region of antibody
- full activation results in the production of a MAC through activation of C9
- end result= lysis of foreign cells (via MAC) |
|
|
Term
opsonins assis in what
what acts as an opsonin? |
|
Definition
phagocytosis
complement- set of blood proteins |
|
|
Term
| if all 9 complement proteins are activated what happens |
|
Definition
| an MAC (membrane attack complex) is formed that drills a hole in pathogens cell membrane |
|
|
Term
| what is the end result of complement? |
|
Definition
| lysis of foreign cells via a MAC |
|
|
Term
| how does activation of complement occur |
|
Definition
| the binding of C1 to Fc (fragment crystallizable) region of antibody |
|
|
Term
| complement acts as ___________________ initially |
|
Definition
| opsonins- they assist in phagocytosis |
|
|
Term
| complement attracts __________, initiates ___________ and __________, and assists in ___________ via ____________ |
|
Definition
| complement attracts PHAGOCYTES, initiates FEVER and INFLAMMATION, and assists in PHAGOCYTOSIS via OPSONINS |
|
|
Term
|
Definition
- occurs when hypothalamus resets to a higher body temp in response to PYROGENS
- higher body temp can control growth of some mesophiles
- may enhance effects of interferon and inflammation and activity of lymphocytes
- enhances beneficial effects of inflammation
- enhances effects of interferons
- inhibits growth of temperature sensitive pathogens |
|
|
Term
|
Definition
|
|
Term
|
Definition
| inflammation, effects of interferons , lymphocyte activity |
|
|
Term
|
Definition
SPECIFIC, ADAPTIVE
- immune response
- results from lymphocytes, B cells, and T cells
- 2 response types:
1. anti body response
2. cell mediated response
- lymphocytes respond to specific antigens through the B- cell receptor and T-cell receptor
- adaptive through immunological memory |
|
|
Term
| how is the third line of defense adaptive? |
|
Definition
| through immunological memory |
|
|
Term
| what are the two types of 3rd line defense responses? |
|
Definition
- antibody response
- cell mediated response |
|
|
Term
| what three cell types are involved in 3rd line defenses? |
|
Definition
| - lymphocytes, B cells, T cells |
|
|
Term
| adaptive immunity _______ and _______ specific invaders while becoming more _________ in the process |
|
Definition
TARGETS AND DESTROYS
EFFECTIVE |
|
|
Term
| antibody response of adaptive immunity/ 3rd line of defense |
|
Definition
| - extracellular pathogens and toxins targeted (bacteria) |
|
|
Term
| cell mediated response of adaptive immunity/ 3rd line of defense |
|
Definition
| - intracellular pathogens are targeted (viruses) |
|
|
Term
| is cell mediated response targeting intra or extra cellular pathogen? |
|
Definition
|
|
Term
| is antibody response targeting intra or extra cellular pathogen? |
|
Definition
|
|
Term
|
Definition
antigen- any substance that causes your immune system to produce antibodies against it. An antigen may be a foreign substance from the environment, such as chemicals, bacteria, viruses, or pollen.
THE PATHOGEN!!!!!! |
|
|
Term
| inflammation causes migration of which leukocytes? |
|
Definition
| neutrophils, monocytes, and lymphocytes |
|
|
Term
| why is complement activation not an effective means of combatting infection from a naked virus? |
|
Definition
| the end result of complement activation is the formation of a MAC (membrane attack complex), without an envelope, the MAC has nothing to bind to !!! |
|
|
Term
| what must be present for a MAC to bind |
|
Definition
|
|
Term
| the third line of defense is the result of the actions of what |
|
Definition
| lymphocytes, b cells, t cells |
|
|
Term
| lymphocytes response to specific antigens how |
|
Definition
| through b- cell receptor and T-cell receptor |
|
|
Term
|
Definition
EXOGENOUS ANTIGEN- toxins, secretions, components of microbial cell walls, membranes, flagella, pili that is CIRCULATING IN THE BODY
(uses MHC II and helper T cell/ CD4)
EXTRACELLULAR antigen |
|
|
Term
|
Definition
| ENDOGENOUS ANTIGEN- pathogens reproduce inside a body's cells and produce this type of antigen. They stimulate a response from the immune system only if they are displayed on the cell membrane. uses MHC I and cytotoxic T cell and CD8 |
|
|
Term
MHC I and CD8 is used when ________ antigens are present
_________ cells are used |
|
Definition
ENDOGENOUS antigens
(intracellular)(from virally infection cell or cancer cell)
cytotoxic T cells |
|
|
Term
MHC II and CD4 is used when _________ antigens are present
________ cells are used |
|
Definition
EXOGENOUS antigens
(extracellular)
helper T cells |
|
|
Term
| what kind of infection would produce endogenous antigens |
|
Definition
VIRALLY INFECTED CELL
CANCER CELL |
|
|
Term
| what kind of infection would produce exogenous antigens |
|
Definition
| it has to be circulating in body, from virus, bacteria, fungi, or toxins |
|
|
Term
| cell mediated response fights mostly against what |
|
Definition
|
|
Term
| antibody response fights mostly against |
|
Definition
|
|
Term
| how are antigens presented |
|
Definition
| on surface of cell membrane/ cell |
|
|
Term
| draw an endogenous antigen of a virally infected cell |
|
Definition
- show viral antigen on surface being displayed by MHC I
- viral antigen= VAg
- cell will be a nucleated cell such as respiratory cell |
|
|
Term
| all cells have MHC 1 or 2? |
|
Definition
|
|
Term
| only which cells have MHC 2 |
|
Definition
| dendritic cells or macrophage |
|
|
Term
| draw an exogenous antigen of a cell that has taken in bacteria via phagocytosis |
|
Definition
- bacterial antigen (bAg) presented by MHC II
-show bacteria being phagocytized and broken down debris as circle with leftover antigens in center that are then presented by MHC II
- must be macrophage or dendritic cell |
|
|
Term
|
Definition
a tissue cell that is present in all tissues that are defensive
- phagocytic cell but NOT LEUKOCYtE |
|
|
Term
| an MHC molecule is used for |
|
Definition
|
|
Term
| who responds to the antigens that are presented by MHC molecules? |
|
Definition
| white blood cells, specifically T CELLS!!!!!! |
|
|
Term
|
Definition
|
|
Term
|
Definition
- have TCR and CD8 on surface
- CD8 recognizes MHC I
- TCR or t cell receptor recognizes antigen
- directly kills cells expressing endogenous antigen |
|
|
Term
|
Definition
|
|
Term
| cytotoxic t cells kill cells expressing (endogenous or exogenous) antigens ? |
|
Definition
| endogenous - virally nucleated infected cell |
|
|
Term
|
Definition
- have TCR and CD4 on surface
- target exogenous antigens being expressed
- help regulate activity of Cytotoxic T cells and B cells
- TCR recognizes antigen
- CD4 recognizes MHC II
- results in formation of TH1 and TH2 cells
- 2 types:
1. TH1- assist cytotoxic T cells and regulate and promote innate immunity
2. TH2- assist b cells |
|
|
Term
| helper T cells target cells expressing (endogenous or exogenous) antigens? |
|
Definition
| exogenous, phagocytic cell |
|
|
Term
|
Definition
| assist cytotoxic T cells and regulate and promote innate immunity |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
- have TCR and CD4 on surface but don't respond like helper T cells
- they repress adaptive immune response and prevent autoimmune disease |
|
|
Term
| what is on surface of regulatory T cells |
|
Definition
|
|
Term
| what represses adaptive immune response preventing autoimmune disease |
|
Definition
|
|
Term
| MHC II selects ______ cells |
|
Definition
|
|
Term
| MHC I selects ______ cells |
|
Definition
|
|
Term
| once T helper cells are selected by MHC II, what happens? |
|
Definition
TH2 and TH1 are made
TH2> B cells> creates memory B cells and plasma cells> plasma B cells produce antibodies (antibody response)
TH1>memory Tc Cells
Active Tc Cells> directly kill target cells (cell mediated)
TH1> memory |
|
|
Term
|
Definition
| B cells, memory B cells, plasma cells |
|
|
Term
|
Definition
Active Tc cells
memory Tc cells |
|
|
Term
| when MHC I selected for Cytotoxic T cells what happens next? |
|
Definition
memory Tc cells form
active Tc cells directly kill cells (with performs and granzymes) |
|
|
Term
|
Definition
- achieve antibody response (t cells are cell mediated)
- antigen specific
- doesn't become activated until it interacts with T helper 2 cells
- proliferates and differentiates once activated
- memory B cells gained (adaptive aspect)
- plasma cells produce antibodies |
|
|
Term
|
Definition
-represented as a Y shaped molecule
- 2 antigen binding sites at top of y
- bottom of y is Fc region- receptor protein
- 5 types:
- antibodies binding to antigens result in consequences known as the functions of antibodies including: oxidation (directly kills), neutralization, agglutination, opsonization, or complement activation |
|
|
Term
| cytotoxic t cells produce which response |
|
Definition
|
|
Term
| when an antibody and antigen interact there are consequences. these are the functions of antibodies... what ar e they |
|
Definition
1. neutralization- when an antibody binds to virus making it so virus cannot bind to its target
2. agglutination- antibodies cause bacterial cells/toxins to clump together
3. opsonization- phagocyte binds to bacterial cell by binding to Fc region of antibody (opsonin facilitates phagocytosis) so this makes phagocytosis easier
4. oxidation- only one that directly kills pathogen, when the antibody binds to bacteria it creates hydrogen peroxide h202 and O3 which kills the cell
5. complement activation- antibody activates C1 and C2 binds to the Fc region of antibody which then activates complement which are a set of blood proteins which result in lysis of foreign cells via a MAC |
|
|
Term
| which antibody function directly kills target |
|
Definition
|
|
Term
| what are perforins and granzymes |
|
Definition
active Tc cells directly kill cells using these
perforin- makes a hole
granzyme- enters and kills cell |
|
|
Term
| explain the importance of helper- t cell activation to the antibody response as well as the cell-mediated response |
|
Definition
1. helper t cells are needed to activate b cells (leading to antibody response)
2. they are also needed to assist in the activation of the cytotoxic t cels (leading to cell mediated response) |
|
|
Term
| explain the importance of lymphocyte differentiation |
|
Definition
differentiation allows for phenotypic differences to occur, changes lead to the formation of plasma cells, active cytotoxic t cells and memory cells. without differentiation cells with these functions would not exist.
* you could not get TH2 and TH1 cells from Thelper cells (th1 activated tc cells, the activated b cells)
*you could not get memory b cells and plasma cells without B cells differentiating
*you could not get active tc cells or memory t c cells if Tc didn't differentiate |
|
|
Term
exogenous antigen- circulating antigen from viruses, bacteria, fungi, toxins
endogenous- intracellular antigen from virally infected cell or cancerous cell |
|
Definition
exo- MHC II, presented by an APC (professional antigen presenting cell/ macrophage, dendritic cell and B cell)
*the t cell that responds: helper t cell; CD4 interacts with MHCII
endo- MHC I, presented by any nucleated cell
*t cell that responds: cytotoxic t cell (TC); CD8 interacts with MHC I |
|
|
Term
| differentiation is a result of phenotypic differences that occur. how are the active Tc cells phenotypically different than the naive Tc Cells? |
|
Definition
| active Tc cells produce performs and granzymes allowing for a different phenotype from the naive cells. the naive cells have the genetic material, but they are not expressing the genes. |
|
|
Term
| 5 classes of antibodies that can be produced as a result of antibody response |
|
Definition
-IgG: this is made in the largest quantity in response to exposure to a particular antigen. it can cross the placenta providing passive immunity to newborn
-IgM: this is the first antibody produced following the first exposure to a particular antigen. it is a large antibody possessing ten antigen- binding sites
-IgA: it is known as the secretory antibody remaining at mucosal membranes once produced. it is present in breast milk.
-IgE: its binding to an antigen may result in an allergic response
-IgD: this antibody is only found as the B cell receptor |
|
|
Term
| once antibodies are produced, antigen- antibody binding causes consequences known as the functions of antibodies |
|
Definition
| -in most cases antigen-antibody binding facilitates other cells or processes to take action and destroy target |
|
|
Term
|
Definition
| antibody made in the largest quantity in response to exposure to a particular antigen. it can cross the placenta providing passive immunity to the newborn |
|
|
Term
|
Definition
| this is the first antibody produced following the first exposure to a particular antigen. it is a large antibody possessing ten antigen-binding sites |
|
|
Term
|
Definition
| it is known as the secretory antibody remising at mucosal membranes once produced (present in breast milk) |
|
|
Term
|
Definition
| its binding to an antigen may result in an allergic response |
|
|
Term
|
Definition
| this antibody is only found as the B cell receptor |
|
|
Term
| which antibody class is made in largest quantity in response to exposure? |
|
Definition
|
|
Term
| which antibody class has the capability of crossing the placenta and providing passive immunity |
|
Definition
|
|
Term
| which antibody is present in breast milk |
|
Definition
|
|
Term
| which antibody is the result of an allergic response |
|
Definition
|
|
Term
| which anybody is found as the B cell receptor |
|
Definition
|
|
Term
| which antibody is the first to be produced following the first exposure, and has 10 binding sites |
|
Definition
|
|
Term
| why is a lag period present during the primary response between exposure to an antigen and the presence of antibodies? |
|
Definition
| a lag period is present because antigen presentation, lymphocyte selection and activation followed by differentiation must take place before any antibodies are produced!! |
|
|
Term
| which antibody is present first in the PRIMARY response? |
|
Definition
|
|
Term
| at what time point following exposure to antigen is the maximum amount of IgG present in the primary response (first exposure)? |
|
Definition
|
|
Term
| which antibody is present first in the secondary response(subsequent exposure)?? |
|
Definition
|
|
Term
| at what time point following exposure to antigen is the maximum amount of iff present in the secondary response? |
|
Definition
|
|
Term
| why is a lag period not seen during the secondary response |
|
Definition
| a lag period is not necessary at this point because memory cells do not require presentation, selection, and activation to become plasma cells. |
|
|
Term
| why do we usually not get infected by the same pathogen more than once |
|
Definition
| once memory cells have been produces, the secondary response is quicker with more antibodies produced in comparison to the primary response. this more efficient secondary response does not allow the pathogen time to cause infection and disease. |
|
|
Term
|
Definition
as a result of the products of an antibody response, we can acquire different types of immunities.
Is it natural or artificial??
- naturally acquired: exposure through natural means (direct contact with someone infected; IgG crossing the placenta; IgA present in breast milk)
-artificially acquired: exposure due to injection (injection of antibody or antigen)
AND is it active or passive?
-actively acquired: active production of antibodies (exposure to the antigen has triggered an antibody response)
-passively acquired: antibodies are present because they were given (immunotherapy, mom providing antibodies to the fetus of newborn) |
|
|
Term
| examples of naturally acquired immunities |
|
Definition
| contact with someone infected; ogg crossing the placenta, IgA present in breast milk |
|
|
Term
| examples of artificially acquired immunities |
|
Definition
| injection of antibodies or antigen |
|
|
Term
| examples of actively acquired immunity |
|
Definition
| active production of the antibodies due to exposure to the antigen which triggers an antibody response (LEADS TO MEMORY CELLS!!) |
|
|
Term
| examples of passively acquired immunities |
|
Definition
antibodies are present because they are given
(immunotherapy, or mom providing antibodies to fetus or newborn) |
|
|
Term
| which immunity leads to the creation of memory cells |
|
Definition
| actively acquired immunities |
|
|
Term
| a pregnant female receives a vaccine within two weeks of giving birth. what type of acquired immunity does she now have? |
|
Definition
artificially active immunity
(its artificial bc of vaccine, active because of memory cells being created due to antibody response) |
|
|
Term
| the antibodies present will cross the placenta and be present in the newborn for a period of time. what type of acquired immunity is this? |
|
Definition
passive natural
(passive, antibodies were given, natural- it came from mother) |
|
|
Term
you have received a potentially fatal snakebite and need something that will provide immediate protection against the venom present in your body. what do you ask for, active or passive immunity? what is your reasoning
a year later, the same type of venomous snake bites you again. based on your answer above, do you have memory cells present specific to the venom? do you need treatment again> |
|
Definition
passive- because the antibodies are given straight away
if it was active then the antibodies would have to be produced and this would require a delay.
no memory cells are not present because it was not an active immunity. treatment is needed again because the initial treatment was not active |
|
|
Term
passive immunization
vs
active immunization |
|
Definition
passive results from immunotherapy, or injection of antibodies for the purpose of treating an infection
active immunization results from vaccination where a controlled exposure to an antigen with the purpose of providing future protection from the same antigen. the introduction of the antigen stimulates a primary response producing memory cells. thus any future exposure results in a secondary response. |
|
|
Term
|
Definition
| made using, whole, living cells or viruses; these pathogens have the ability to reproduce but they have been modified so that they lack virulence |
|
|
Term
| how are the antigens altered in attenuated vaccine |
|
Definition
they are altered so that they do not have virulence
(but they still can replicated and result in memory cells) |
|
|
Term
|
Definition
| made using whole, but dead, cells or viruses or portions of the cell/virus |
|
|
Term
| which type of vaccine uses dead cells |
|
Definition
|
|
Term
|
Definition
| made using a modified toxin |
|
|
Term
| if a baby is born with an acquired immunity, why is vaccination still necessary? |
|
Definition
because the acquired immunity was passive, meaning that there was no memory cells made, the antibodies were given when they crossed the placenta or through breastmilk.
so... we must give a vaccine to allow their immune system to respond and create memory cells. |
|
|
Term
| which vaccine type best mimics a real disease? |
|
Definition
|
|
Term
| one advantage that the inactivated and toxoid vaccines have over the attenuated? |
|
Definition
| they are safer because the pathogen is not alive!! |
|
|
Term
| why are multiple exposures to the antigen necessary to achieve and maintain memory for inactivated and toxoid vaccines, whereas one exposure is often sufficient for attenuateD? |
|
Definition
| the attenuated vaccine consists of an organism that is able to increase in number in the host. This allows the immune system to respond over time creating a better response. the inactivated and toxoid vaccines introduce only what is present in the injection. multiple exposures (injections) are necessary to introduce enough antigen to get a good immune response. |
|
|
Term
|
Definition
|
|
Term
| for toxoid vaccine immune response is against what |
|
Definition
|
|
Term
|
Definition
These vaccines combine antigens from several
toxoids and inactivated pathogens that are administered
simultaneously. Examples include MMR—vaccine against
measles, mumps, and rubella—and Pentacel, which is a vaccine
against diphtheria, tetanus, pertussis |
|
|
Term
|
Definition
goal is to improve existing vaccines and develop new vaccines
ex:
produce large quantities of pure bacterial or vial antigen
genetically alter microbe to express antigen of interest and act as a live vaccine
For example, scientists have developed a
recombinant DNA vaccine against a fungus, Blastomyces (blas-to
.
-
mı
.
´se
.
z)—the first vaccine against a fungal pathogen. Scientists
can also use a variety of genetic recombinant techniques to make
improved vaccines. For example, they can selectively delete
virulence genes from a pathogen, producing an irreversibly
attenuated microbe, one that cannot revert to a virulent pathogen |
|
|
Term
| how can vaccines be unsafe |
|
Definition
- mild toxicity leading to pain at injection site
- anaphylactic shock (allergic reaction to vaccine)
- residual virulence |
|
|
