Ch. 8 - Adaptive Immunity Flashcards

(52 cards)

1
Q

Define and explain the role of the following cells and/or substances in activating the immune response:

Macrophage

A

This is an antigen presenting cell

It is second most effective in comparison to dendritic cells

–> critical in secondary response!!!

Activated Th cell by releasing IL-1

It also is able to phagocytize and turn into super macrophage (can phagocytize more than neutrophils)

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2
Q

Define and explain the role of the following cells and/or substances in activating the immune response:

Dendritic Cells

A

This is an antigen presenting cells

Most EFFECTIVE at preventing antigens to naive Th cells

Important in initiating PRIMARY response

Found in most tissue but mainly in tissue interfacing with the environment

Phagocytic and then migrate to T cell rich lymphoid tissues to ensure activation of immune response

Release IL-1 to activate Th cells

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3
Q

Define and explain the role of the following cells and/or substances in activating the immune response:

Helper T

A

Th cells = CD4 cells

Once activated proliferate into Th1 or Th2 cells.

Can suppress each others function making it either more humoral or more cell mediated

Th1 = Releases IL-2 –> stimulates proliferation of cytotoxic t cells and NK cells

Th2 = Releases IL-4 and 6 –> stimulated the production of B lymphocytes to plasma and memory cells

also releases IL-5 which stimulates the proliferation of eosinophils and b cells

Th17 = releases Th17,21,22 –> augments inflammation

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4
Q

Define and explain the role of the following cells and/or substances in activating the immune response:

Suppressor T cell

A

Also known as Treg cell

Secretes IL-35 and TGF Beta

Decreases Th1 and Th2 activity

It is involved in providing peripheral tolerance –> suppresses recognition of forbidden clones of T or B lymphocytes from responding against self antigens

Role is to control and limit immune response to self tissues

As we age, we develop more antibodies against our own tissues; T reg is probably losing its effectiveness

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5
Q

Define and explain the role of the following cells and/or substances in activating the immune response:

Interleukin 1

A

IL1 is released from macrophage and dendritic cells that stimulate proliferation of Th to Th1 and Th2.

It is also a pyrogen!

Along with IL6 it also forms acute phase proteins from the liver like complement and clotting factors

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6
Q

Define and explain the role of the following cells and/or substances in activating the immune response:

Interleukin 2

A

This is released from Th1 cell to cause proliferation and maturation of Tc cell and it also stimulates the NK cells

Th1 releases IFN (interferons) to suppress Th2

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7
Q

Define and explain the role of the following cells and/or substances in activating the immune response:

Interleukin 4

A

This is released from Th2 cells to cause proliferation and maturation of B lymphocytes into plasma cells and memory cells.

This also suppresses Th1 cells

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8
Q

Define and explain the role of the following cells and/or substances in activating the immune response:

Interleukin 6

A

This is released from Th2 cells to cause the proliferation and maturation of B lymphocytes into plasma and memory cells

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9
Q

Define and explain the role of the following cells and/or substances in activating the immune response:

IL-10 and TGF Beta

A

Secreted by Th and B lymphocytes

it regulates inflammation and inhibits cytokine production

TCG Beta is secreted by T reg cell –> it inhibits Th1 and Th2 activity

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10
Q

Define and explain the roles of the following cytokines in the inflammatory response.

MIF

A

MIF - Migrating Inhibitory Factor

it’s an important regulator of innate immunity

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11
Q

Define and explain the roles of the following cytokines in the inflammatory response.

MAF

A

MAF= macrophage activating factor increases phagocytosis

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12
Q

Define and explain the roles of the following cytokines in the inflammatory response.

TNF beta

A

TNF beta - Macrophages: tumor necrosing factor alpha stimulates an increase of fibrinogen and others

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13
Q

Define and explain the roles of the following cytokines in the inflammatory response.

Interferon

A

Interferon: secreted from viral infected cells

it warns other cells of infection and causes them to secrete antiviral proteins as well as nucleases

doesn’t protect the already infected cell

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14
Q

Define and explain the roles of the following cytokines in the inflammatory response.

VEGF and PDGF

A

Both of these stimulate endothelial growth to promote healing

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15
Q

Innate Immunity

A

This is the immunity that is there all the time. It is not specific. It has an immediate response.

Includes first two lines of defense (physical barriers and inflammation)

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16
Q

Active Acquired Immunity

A

Result of an immune response to infection or immunization

Slower acting than Innate

Very specific in its targeting

Very long lived (generally)

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17
Q

Passive Immunity

A

Performed antibodies given to a host from a donor (gamma globulin shot)

Preactivated Tc cells given to host

Antibodies from colostrum to newborn (IgA); some protection from IgG for 1st 24 hrs

Antibodies transferred across placenta (IgG)

Memory T and B cells are NOT PRESENT

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18
Q

Primary Immune Response

A

Lag time take 5-7 days; initially releases IgM antibodies

Lag time is due to:

a) antigen processing and presentation
b) clonal selection
c) induction of the Th cells
d) Th cells interacting with B and T cells
e) Maturation and proliferation of B and T cells
f) Production of antibodies, migration of activated Tc cells to blood

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19
Q

Secondary Immune Response

A

Takes 24 hrs; MOSTLY IgG with a little IgM

a) produces large amount of antibodies in 24 hrs
b) memory cells are already selected, differentiated, and there are large numbers of them
c) Some memory cells have undergone a class shift and are producing IgA antibodies for surface protection and prevention

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20
Q

Humoral Immune Response

A

Mediated by B lymphocytes

Three kinds of cells:

  1. Immunocompetent B cells “processed through bursa equivalent tissue” –> bone
  2. Plasma cells secrete antibodies
  3. Memory B cells: responsible for rapid secondary response
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21
Q

Cellular Immunity

A

Involves 5 types of T lymphocytes

  1. Th
  2. Treg
  3. Tc
  4. Td (lymphokine secreting)
  5. memory cells for each type
22
Q

Define/differentiate functional differences between each of the following white blood cells of the specific immune response.

Helper T lymphocytes (Th1 and Th2) - CD4 cells

A

CD4 cells (Th cells)

Once presented the antigen, naive Th cells proliferate and differentiate into either Th1 or Th2

*Th1 or Th2 can suppress each others function, causing an immune response to be more dominantly humoral or cellular

Th1 –> releases IL-2 which causes the proliferation of Tc and NK cells

Th2 –> releases IL-4 and IL-6 which cause the proliferation of B lymphocytes into plasma cells and memory cells

23
Q

Define/differentiate functional differences between each of the following white blood cells of the specific immune response.

Cytotoxic T lymphocyte (Tc) - CD8

A

Direct cellular killing of target cells by attaching and secreting perforin and granzymes. Perforin forms holes, granzymes enter and activate capaces initiating apoptosis.

CD8 Tc cell is MHC class 1 restricted and kills cells with class 1 MHC markers

Targets:

a) virally infected cells
b) Tumors expressing MHC 1
c) foreign grafts
d) Bacteria

24
Q

Define/differentiate functional differences between each of the following white blood cells of the specific immune response.

Lymphokine secreting T lymphocytes (Td)

A

Delayed hypersensitivity. Lymphokine secreting, involved in inflammation and inducing and regulating macrophage function and other not well delineated.

(MIF, MAF, TNF beta)

25
Define/differentiate functional differences between each of the following white blood cells of the specific immune response. Treg
Secretes IL-35 and TGF Beta both decreases Th1 and Th2 activity Involved in providing peripheral tolerance ex) suppresses recognition of forbidden clones of B or T lymphocytes from responding against self antigens Role is to control and limit immune response to self tissues --> as we age we develop more antibodies against our own tissues; Treg protection is probably slowly losing its effectiveness
26
Define/differentiate functional differences between each of the following white blood cells of the specific immune response. Memory lymphocytes
These are what allow our body to have a secondary immune response within 24 hours; will be mosly IgG with a few IgM --> some may class shift into IgA and protect surface
27
Define/differentiate functional differences between each of the following white blood cells of the specific immune response. B lymphocytes
B lymphocytes are capable of becoming either plasma cells or memory B cells. Mature and undergo directed proliferation and differentiation in bone marrow Each B cells only responds to one specific antigen --> when activated becomes a plasma cell --> or memory cells capable of causing a secondary response Present to Th cells in order to accelerate Humoral response
28
Define/differentiate functional differences between each of the following white blood cells of the specific immune response. Plasma Cells
Plasma Cells: antibody secreting Function of antibodies: a) neutralizing bacterial toxins b) agglutination --> facilitates destruction c) neutralizing viruses --> by binding to their binding sites can't bind to target cells d) neutralizing bacteria's ability to damage our cells directly e) Activating complement and inflammation cascade f) opsonization - attracts macrophage and facilitates phagocytosis
29
Define: Antigen and the requirements for a molecule to elicit an immune response.
Antigen: capable of inducing the formation of components for the immune system Needs to be: a) Sufficiently foreign to the host (not recognized as self) b) Sufficiently large ex) Hapten --> penicillin bound to protein c) Sufficiently complex d) Present in sufficient amounts
30
Briefly describe the process of antigen processing, the roles of Antigen Presenting Cells, (APCs) and the role of MHC markers in the process.
Antigen Presenting Cells: a) Dendritic Cells - most effective at presenting antigens to naive Th cells; important in initiating primary response - -> found in most tissue but are abundant in tissue interfacing with the environment - -> phagocytic, then migrate to T cell rich lymphoid tissues to ensure activation of immune response b) Macrophage - next most efficient, critical secondary response c) B-lymphocytes - present to Th cells in order to accelerate humoral response MHC --> glycoproteins found on the surface of all human cells with the exception of RBC's Antigen processing involved combining the MHC complex with an antigen after phagocytosis, then placing the MHC antigen complex on the surface of the presenting cells to signal Th, Tc, and B cells MHC marker (two types) 1. MHC class 1 - generally present endogenous antigens from inside the cells --> often viral infected cells or cancer cells --> Tc cells target these markers 2. MHC class 2 - generally presents exogenous antigens; developing class marker class II go to lysosome where it attaches exogenous antigens from digested microbes --> can be presented to B and T lymphocytes to activate the immune response
31
Differentiate the roles of MHC class I vs MHC class II markers in antigen processing and which immune cells respond to changes or antigens displayed on MHC I or MHC II markers
1. MHC class 1 - presents endogenous antigens on MHC class 1 marker (its often viral infected cells or cancer cells) --> Tc cells target and destroy 2. MHC class 2 - presents exogenous antigens, goes to lysosome to pick up antigens from digested microbes --> goes to B and T lymphocytes to activate the immune response
32
Delineate which cells are capable of being APCs and which are the most effective
Dendritic cells, macrophages, and B lymphocytes are capable of being APCs' Most effective are Dendritic Cells!!!
33
Describe the concept of tolerance and differentiate the difference between Central Tolerance vs Peripheral Tolerance. Explain when central tolerance was developed and what constitutes peripheral tolerance. Explain which WBC provides Peripheral Tolerance and how.
Tolerance: no immune response to a particular antigen, especially self-antigen. the antigen doesn't trigger an immune response. Central tolerance - during development phase of B and T cell clones in the fetus, there was rapid rearrangement of VJ and VDJ genes which produced receptors for the Fab portion of antibodies and Tc cells. If developing T or B cell populations or clones T cell receptor or B cell receptor bind to self antigens, the cells are deleted or caused to undergo apoptosis Peripheral Tolerance - limited number of forbidden clones of either B or T lymphocytes persisted, these are actively suppressed from activating into an immune response by Treg lymphocytes
34
What are the Fab and Fc portions of antibodies?
Fab = heavy and light chains determine 1. binding specificity to antigen 2. binding activates FC portion Fc = crystalline fragment responsible for... 1. Biological functions - -> activation of inflammation - -> activaiton of complement 2. Transport of maternal antibodies across the placenta by trophoblasts
35
IgM
Antibody produced during the primary response!!! Agglutination is very powerful! Complement activation
36
IgG
Major class of secondary response 80-85% of circulating antibodies, most abundant antibody Precipitation, agglutination, complement activation Crosses the placental membrane through trophoblasts; major antibody in placental and fetal blood
37
IgA
Secretory immunoglobin (urinary tract, lungs, mouth, tears, sweat, breast milk) Used to prevent infections and prevents host from being a carrier Preventative antibody prevents bacterial and viral infections Lymphocytes circulate through a different group of lymphoid tissues
38
IgE
with eosinophil it is primary weapon against parasites Fc portion binds to mast cells when locally activated by parasitic antigens, triggers mast cell degranulation unfortunately, inappropriate class switch may activate IgE against allergens, cause of allergic responses by inappropriate mast cell degranulation
39
IgD
Located primarily on the surface of B lymphocytes, functions as one type of B cell receptor other functions are unknown
40
Define/differentiate: Immuno-incompetent vs Immuno-competent. Explain when a T or B lymphocyte transitions from Immuno-incompetent to Immuno-competent
Immuno-incompetent = B or T cells is immature an unable to recognize foreign antigens and elicit an immune response Immunocompetent = B or T cell is mature and capable of recognizing foreign antigens and eliciting an immune response Transition for B cells occurs in bone marrow Transition for T cells occurs in Thymus
41
Be prepared to discuss the processes occurring in Immuno-incompetence and Immuno-competent phases of the development of the immune system in a infant prior to birth and immediately post-partum. The fetus will have central tolerance when immuno incompetent cells are destroyed if they bind to a self antigen before maturation If the forbidden clones escape T reg keeps it under control so the baby won't have problems
1. Cell mediated immune response (Tc) develops early in gestation and is fully functional at birth 2. Humoral mediated immune response if clearly deficit although a fetus can produce IgM antibodies by 3rd trimester --> at birth baby's ability to produce antibodies, phagocytic activity, activate compliment is clearly deficit --> trophoblasts actively transport IgG antibodies from mother blood across placenta to fetal circulation --> maternal antibodies remain in fetal circulation for up to 5 months --> antibodies in colostrum can only cross for 24 hrs after the baby is born but antibodies present in GI tract provide some protection --> gut and oral IgA protection for nursing mothers
42
Describe how and the mechanisms involved to immunologically protected a newborn during the first few months of its life. How, when and where did the immunoglobins come from. Describe the function of trophoblast cells.
1. Cell mediated immune response develops early in gestation and is fully functional at birth 2. Humoral mediated immune response is not fully functional at birth --> fetus may produce IgM antibodies by 3rd trimester, at birth the baby's ability to produce antibodies, phagocytic activity, and activate complement is clearly deficit 3. Trophoblasts actively transport IgG antibodies from mother blood to fetus 4. Maternal IgG antibodies may remain in fetal circulation for up to 5 months 5. Antibodies in colostrum may only cross for 24 hours after baby is born 6. Gut and oral IgA protection --> provided preventative surface protection if mother breast feeds
43
In terms of objective number 7, describe the problem involved with a Rh- mother bearing a Rh+ baby. Relate this problem to primary vs secondary responses.
The problem with this is the mother will recognize her baby's antigens as foreign and will produce an primary response against it 1. In primary response just IgM antibodies are produces and can't cross the placental barrier Sadly, the secondary immune response will kick in which involved IgG antibodies, these can cross the placental barrier and cause damage and death to fetus
44
Explain the role of the thymus and the bone marrow (other lymphoid tissues) in the development and maintenance of the immune system from infancy to old age.
Immuno-incompetent cells maturate in the bone marrow and thymus to form immunocompetent cells capable of eliciting an immune response. As a person ages, the thymus decreases in shape and function, this doesn't decrease T cell numbers but their function There is also a decreased in specific antibody production as a person ages as well as decreased number of circulating memory b cells Autoantibodies increase with age!!
45
Define/differentiate: Primary Immune response VS Secondary immune response. Delineate all the factors that contribute to the “lag time” of the primary response. Explain why is there relatively no “lag time” in the secondary response. Delineate which antibodies are predominantly secreted in the 1o vs 2o response.
Primary immune response ---> lag time is 5-7 days; primarily IgM Lag time is long because: 1. antigen processing and presentation 2. clonal selection 3. induction of Th cells 4. Th cells interacting with B and T cells 5. Maturation and proliferation of B and T cells 6. Production of antibodies, migration of activated Tc cells to blood There are NO MEMORY CELLS Secondary immune response -> lag time is 24 hrs; primarily IgG with some IgM and potentially class switch to IgA MEMORY CELLS MAKE IT SO LAG TIME IS SHORT
46
Define/differentiate: Exudation, Margination Diapedesis, Chemotaxis
Exudation - movement of plasma and proteins out of vessels --> occurs during acute inflammation Margination - adherence of the WBC's to the capillary endothelial membrane Diapedesis - the WBC squeeze out of vessel to inflammation site Chemotaxis - what causes cells to come to the inflammatory site for neutrophils --> mast cells and complement release chemotaxic properties to draw them to inflammatory site for eosinophils --> mast cells release chemotaxic properties to draw eos to site
47
Define/differentiate: Phagosome and phagolysosome
Phagosome - what has been phagocytized into the cell and is now contained Phagolysozyme - the fusion of the phagosome with the lysozyme to cause destruction of whatever was phagocytized = digestion
48
Explain what causes a fever in an infected host. Delineate which cells secret pyrogens that are responsible for fever. Name two pyrogens. Describe the theories as to the function of a fever during an infection.
Fever is caused by IL-1 --> targets hypothalamus and increases body temperature - released from macrophages and dendritic cells It raises body temperature to prevent bacterial growth It also prevent iron from being used by bacteria Fever can be detrimental by causing the gram - endotoxins to become more potent leading to human protein denaturing
49
Elucidate the role of lactoferrin in the inflammatory response and indicate its source.
Lactoferrin is released from neutrophils to prevent uptake of iron in bacteria.
50
Describe the role of α Antitrysin in the immune response and describe the effects of the inherited disease, α-antitrysin deficiency.
A antitrypsin is produced by the liver and prevents protease damage During immune response, lysis of the phagocyte releases protease and can do a lot of collateral damage, alpha antitrypsin would protect against this lack of a antitrypsin would mean collateral damage
51
Be prepared to discuss ways in which the inflammatory process may become counter productive and even destructive to a patient.
It can become destructive when there is no control over postivie feedback ex) compliment, coagulation cascade, and kinin system The biochemicals of each protein system is so potent that it can be lethal if not confined to tissue with problem.
52
In general, be able to describe the inflammatory and immune response to an infection in sequence from the onset of the infection to the destruction of the foreign invaders.
Look at picture drawn in yellow notebook. Draw it out. 1. Compliment is either activated by antigen antibody complex = classical or bacterial polysaccharides - could also be activate by bacterial carbs which would be lectin pathway 2. Compliment triggers Mast cell degranulation 3. Mast cell degranulation release histamine, cytokines, neutrophil chemotaxic factors, esoinophil chemotaxic factors, leukotrienes, prostaglandin E, VEGF/PDGF, and PAF --> results in increased capillary permeability and vasodilation 4. Neutrophils are first to site due to mast cell release of neutro chemotaxic factor - -> phagocytize to an extent but not near as well as macrophages - -> release monocyte chemotaxic factor 5. Monocytes come and turn into macrophages --> these eat everything and lots of it - -> can fuse into one big super macrophage - --> processes antigens onto MHC 1 marker 6. Eosinophils are brought to sight by eosinophil chemotaxic facter as well as IgE FC portion activated against parasites - -> help to control inflammation - -> biggest protection against parasites 7. Basophils come and turn into mast cells 8. Dendritic cells are also phagocytizing --> critical in primary response --> process antigens on MCH 1 marker 9. Dendritic cells/Macrophages go to lymph nodes and present to Th --> activated Th by releasing IL-1 10. Th cells activated into Th1 and Th2 11. Depending on t cell receptor fit to antigen presentation depends on which response is more dominant 12. Th1 cells release IL2 which activated Tc and NK 13. Th2 releases IL4 and IL6 which activated B lymphocytes to B memory and plasma cells 14. Primary response will mostly secrete IgM antibodies (secondary will be IgM) 15. Tc start killing by injecting perforin and granzymes into any cell that has MHC 1 marker 16. NK cells destroy any cell down regulating MCH 1 marker ex) cancer cells 17. Memory cells are being produces for secondary response which will occur in 24 hr instead of 5-7 days