Module 3 Flashcards

1
Q

5 phases of adaptive immune response

A
  1. Antigen recognition
  2. Lymphocyte activation
  3. Eliminations of pathogens
  4. Contraction
  5. Memory
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2
Q

Antigen recognition

A

-after pathogen has entered body and and evaded innate immune defences, PAMPs are seen by antigen-presenting cells (APCs)
-APCs will present antigens to naive T-cells via their surface MHC proteins

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3
Q

Lymphocyte Activation

A

-requires a series of cellular interactions which lead to T-cell and B-cell differentiation and clonal expansion

Bcells -> plasmocytes
Tcells -> Cytotoxic T-cells

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4
Q

Eliminations of Pathogens

A

-depending on type of pathogen invading, most efficent defenses are unleashed: Hummoral or Cell-mediated

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5
Q

colonal Expansion

A

production of a large quantity of identical cells from the same original cell

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6
Q

Hummoral elimination of pathogens

A

plasmocytes produce antibodies that bind to extracellular pathogens

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7
Q

cell-mediated elimination of pathogens

A

cytotoxic t cells destory cells infected by intracellular pathogens or get activated by antigens presented by APCs

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8
Q

contraction (apoptosis of immune cells)

A

Once the pathogen is eliminated, the vast majority of activated lymphocytes undergo apoptosis and the immune response gradually declines

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9
Q

apoptosis

A

programmed cell death that occurs in a way controlled by the cell itself, which generate alsmost no damage to surrounding area

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10
Q

establishment of immunological memory

A

the few immune cells that survive the contraction phase differentiate into memory cells

When re-exposed to the same antigen, these memory cells proliferate quickly to generate an immune response much faster and more robust

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11
Q

which processes are induced in lymphocytes during their activation?

A

differentiation and clonal expansion

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12
Q

the role of MHC molecules

A

-helps identify and recognize self from non-self molecules to ensure IS does not attack the host
-display antigenic peptides on the surface of cells
-this can be recognized by TCR and co-receptors (CD4 or CD8) to initiate an adaptive imune response, which leads to elimination of foreign antigens

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13
Q

Classification of MHC molecules

A

MHC class I and MHC class II

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14
Q

MHC class I

A

CD8 cytotoxic cell

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15
Q

MHC class II

A

CD4 helper T cell

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16
Q

hoew do T cells recognize pathogens

A

cannot recognize extracellular pathogens by themselves they require an intermediate to present them

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17
Q

how do APCs internalize pathogens

A

phagocytosis OR receptor-mediated endocytosis and process them into peptides (antigens) and displayed on the MHC on the surface and are recognized by T cells

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18
Q

Receptor-mediated endocytosis

A

an endocytic process in which a cell absorbs external material by invagination of the plasma membrane. This process relies on receptors specific for the material being absorbed

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19
Q

two types of APCs

A

professional and nonprofessional

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20
Q

Professional APCs

A

MACROPHAGE, B CELL & DENDRITIC CELL

most efficent cells that both present antigens through MHC class II and express cosimulatory signals to activate helper T cells

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21
Q

nonprofessional APCs

A

other cell types can be inducedto express MHC class II complexes or stimulatory molecules, but normally they dont. This isbecause these cells will rarely be needed in this specific function and only for short periods of time in case of sustained inflammatory response

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22
Q

examples of nonprofessional APCs

A

fibroblasts and glial cells

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23
Q

the two pathways that lead to the formation of surface cell complexes

A

endogeneous and exogeneous

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24
Q

endogenous pathway

A

forms peptide MHC class I recognized by CD8 cytotoxic T cells

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25
Q

exogenous pathway

A

form peptide MHC class II recognized by CD4 helper t cells

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26
Q

Antigen processing by the endogenous pathway

A

-allows cell to proccess self or foreign intracellular particles and present them at the cell surface in order to be recognized by T cell receptors of cytotixic T cells

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27
Q

Why would cells need to present intracellular particles to the immune system

A

degrading self or foreign elements into peptide fragments which are transported to ER to associate with MHC class I. this complex is transported to golgi complex, further processed and transported to surface

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28
Q

5 main steps in the process of exogenous antigen presenting

A
  1. Antigen engulfment
  2. proteolytic processing
  3. Formation of MHC-antigen complex
  4. cell surface expression
  5. recognition by helper T cell
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29
Q

Exogenous: Antigen engulfment

A

antigen presenting cells engulf the foreign antigen by endocytosis forming and endosome. The antigen is generally recognized by PRRs

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30
Q

Exogenous: Proteolytic processing

A

Foreign antigens inside the endosome are broken down into fragments by proteolytic processing

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31
Q

what is proteolytic processing

A

protease cleaves one or more bonds in a target protein to modify its activity (activation, inhibition or destruction of activity)

32
Q

Exogenous: formation of MHC-antigen complex

A

the vesicle containing the foreign fragments fuses with vesicles containing MHC molecules (originating from the endoplasmic retitculum via the golgi) forming MHC-antigen complexes

33
Q

exogenous: cell surface expression

A

the MHC-antigen complex is transported to the plasma membrane, where it will be displayed on the surface of the cell

34
Q

exogenous: recognition by helper T cell

A

the t cell receptor (TCR) on teh surface of a helper t cell binds to the MHC-antigen complex on the cell surface of the APC, which will initiate an adaptive immune response

35
Q

B-cell Receptor (BCR)

A

the BCR is composed of a membrane-bound antibody and signal transduction molecules (ITAMs). BCRs recognize and bind to extracellular pathogens or toxins directly

36
Q

ITAMs

A

an immunoreceptor tyrosine-based activation motif is composed of a repeated sequence of four amino acids in the cytoplasmic tails of cell surface proteins

37
Q

T cell receptor (TCR)

A

-TCR complex is formed of a membrane bound antigen-specific molecule and signal transduction molecules
-TCRs in association with a co-receptor (CD4 or CD8) recognize and bind ti peptide MHC complex

38
Q

CD4 co receptors are expressed on _________ cells, which recognie peptide MHC class ___________

A

Helper T cells, MHC class II

39
Q

CD8 co receptors are expressed on _________ cells, which recognie peptide MHC class ___________

A

cytotoxic T cells, MHC class I

40
Q

Lymphocyte Activation

A

involves many interactions with other immune cells, which will mediate the efficency of the specific immune response

41
Q

cells involved in lymphocyte activation

A

macrophage, dendritic cell, b cell, helper t cell, cytotoxic t cell

42
Q

cytokine networks

A

coordinate appropriate immune responses and modulate the balance between humoral and cell-mediated immunity

43
Q

classes of cytokines depdndent on function and structure:

A

-chemokines
-interleukins
-interferons
-tumor necrosis factor
-growth factors

44
Q

what does the immune system require to stimulate hummoral immunity and differentiation of B cells

A

CD4 helper T cells

45
Q

two categories of antigens acle to activate B cells

A

thymus-dependent and thymus-independent

46
Q

thymus-independent antigens

A

few antigens that can induce the production of antibodies by B-cells without the presence of a T-cell

47
Q

T-cell dependent B cell activation

A

involves specific signals essential to the productionof functional plasmocytes and memory B-cells. This interaction induces an exchange of singals between 2 lymphocytes allowing activation of hummoral response

48
Q

steps leading to signals in the process of B cell activation

A
  1. Peptide-MHC class II complex
  2. Signal 1: TCR- peptide:MHC complex
  3. expression of cosimulatory molecules
  4. Signal 2: Cosimulation
  5. Signal 3: Cytokines
  6. outcome of three signals
49
Q

how many signals lead to b cell activation and what are they

A
  1. TCR-peptide:MHC complex Class II
  2. Cosimulation
  3. Cytokines
50
Q

Step 1 of b cell activation

A

peptide-MHC class II complex

as the antigen binds BCR on a specific B cell does not produce a strong enough signal to activate the cell, the antigen is internalized by receptor-mediated endocytosis, processed and displayed on the cell membrane as MHC

51
Q

At what stage does the B cell acting on APC express a high level of peptide: MHC complex on their cell surface

A

step 1

52
Q

Step 2 b cell activation

A

Signal 1: TCR-peptide: MHC complex

the specific TCR complex and CD4 co-receptor on the T cell recognizes and binds to peptide: MHC complex on B cell

53
Q

Step 3 b cell activation

A

expression of cosimulatory molecules

Signal 1 induces the expression of CD40L on the cell surface of the helper T-cell

54
Q

Step 4 B cell activation

A

Signal 2: Co-stimulation

CD40L and CD28 expressed on the T-cell, respectively, bind to CD40 and B7 expressed on the V-cell inducing a costimulatory signal in both cells

55
Q

The immune synapse structure

A

t-cells will not become properly activated if only signal molecules such a t-cell receptor and a peptide:MHC complex interaction. a immune synapse consisting of signal molecules AND adhesion proteins must be formed

56
Q

what is an immune synapse

A

interaction between a t-cell and a APC

57
Q

three components of an immune synapse

A
  1. Signal molecules (cSMAC)
  2. Adhesion molecules (pSMAC)
  3. signal regulation molecules (dSMAC)
58
Q

signal molecules (cSMAC) in immune synapse

A

the central SMAC contians the molecules responsible for signalling between the two cells such as the TCR and peptie:MHC molecules

59
Q

adhesion molecules (pSMAC) in immune synapse

A

the peripheral SMAC contains adhesion proteins, auch as integrins and cytoskeletal linker proteins, responsible for keeping the cells in contact long enough for signals to propogate

60
Q

signal regulation molecules (dSMAC) in immune synapse

A

the distal SMAC consists of proteins with large extracellular domains that are responsible for helping regulate signal transduction

61
Q

pattern of immune synapse

A

“bullseye” with three rings depicting three different cell clusters (SMAC). other immune synapses can be arranged differently

62
Q

Function of Immune Synapse

A

Primary goal: effective activaton of the T cell

  • holds signal proteins together to form stronger connections, giving enough time for right amount of signals

-reorganization structures inside the t cell, directing the release of cytokines close to target cell

-regulates lymphocyte activation

63
Q

Chemokines

A

-induce chemotaxis
-call in cells to the region of infection
-play a key role in inflammation, cell mediated and hummoral responses and hematopoiesis

64
Q

Interleukins

A

-contain over 10 subfamilies
-regulate immune and inflammatory responses
-primarily affect the proliferation and differentiation of various hematopoietic and immune cells

65
Q

Interferons

A

-the most common and well-known interferon molecules are IFN-apla and IFN-y

-induce antiviral state - inhibit the replication process of virsus

  • helps regulate immune responses
66
Q

Tumor Necrosis Factor

A

-most common are TNF-alpha and TNF-beta

-involved in systemic inflammation (septic shock)

-involved in tumor regression

-can cause apoptosis (cell death)

67
Q

Growth Factors

A

-stimulate: growth, proliferaition, healing, cellular differentiation

-regulate a variety of cellular processes such as immune responses

68
Q

what is the outcome of B cell activation:

A

proliferation and differentiation into plasma and memory B cells

69
Q

what is imunological memory

A

the ability of lymphocytes to respond more efficently to re-infection by a previously encountered antigen

70
Q

when does immunological memory occur

A

when there is a second encounter with an antigen that induces a hightened state of immune reactivity, mediated by memory B cells

71
Q

why do we get the flu multiple times if memory cells last for decades

A

due to different strains

72
Q

memory B cells vs naive B cells

A

memory B cells differentiate from naive B cells and display the same membrane-bound antibody as parent cell

*memory b cells have longer

73
Q

how do memory b cells work fast than naive b cells

A

naive b cells need to be activated through series of cell interactions (like antigen presentation) before they can differentiate into plasma cells and memory cells. memory cells can differentiate immediately into plasma cells making them faster

74
Q

Natural Passive Immunity

A

-acquired by the fetus or newborn from the mother
-placental transfer of antibodies during pregnancy or breastfeeding
-short lived (6 months)
-no immunological memory for reciepent

75
Q

Artificial passive immunity

A

-acquired by injection of serum containing antibodies
-immunity is temporary
-no immunological memory for reciepnt

76
Q

Natural active immunity

A

-acquired through infection by a pathogen possibly leading to symptoms
-development of innate and adaptive immune responses
-immunological memory has significant change of being developed

77
Q

Artificial Active Immunity

A

-acquired through vaccination
-development of innate and adaptive immune responses
-normally no symptoms
-imunological memory has significant chnage of edveloping