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Immunology > Innate and Adaptive Immunity > Flashcards

Innate and Adaptive Immunity Flashcards

1
Q

Immune response - process

A
  1. Microbe penetrating body epithelia aka skin
  2. Neutrophils - 1st to infection site
  3. Monocytes differentiate into macrophages
  4. Macrophages utilizing surface receptors PRRs - that recognize and bind to pathogen.
  5. Macrophages activated and secrete cytokines and hemokines - causes inflammation
  6. Cytokines - >’s permeability of Bvs, increases adhesive properties of bvs - initiate inflammation
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2
Q

Which cells are first to infection site?

A

Neutrophils

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3
Q

In step 6 of immune response, cytokines are activated by macrophages thereby causing inflammation, what else triggers inflammation?

A

Complement ;
• Complement coats microbial surfaces with fragments that are recognised and bound by phagocytic receptors on macrophages

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4
Q

Cytokines and complement fragments cause circulating neutrophils to migrate to site of infection, cytokines attract them there. (T/F)

A

False; Cytokines and complement fragments cause circulating leucocytes to migrate to site of infection, chemokines attract them there.

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5
Q

List cells involved in Adaptive Immune System

A

B cell, T cell, Antibodies, CD4+ T cell, CD8+ T cell, gamma delta T cell, Natural killer T cell

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6
Q

Functions of Adaptive Immune System:

A
  • Recognition of specific “non-self” Ags among “self” Ags
  • Elimination of specific pathogens or pathogen-infected cells
  • Development of an immunologic memory – quicker elimination of pathogen upon reinfection
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7
Q

Main cells of Adaptive Immune System

A

T and B cells

B cell receptor is membrane bound

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8
Q

Adaptive Immune System - role

A

Generates large numbers of preexisting receptors expressed on lymphocytes, that can identify essentially any Ag

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9
Q

Three molecule groups specifically recognize foreign Ag (adaptive immune sys) , what are they?

A

T cell receptor (TCR)
B cell receptor (BCR)
Major Histocompatibility Complex (MHC)

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10
Q

Major Histocompatibility Complex (MHC) - cluster of genes in humans is?

A

Human Leukocyte Ag (HLA) in humans

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11
Q

The MHC molecule is always bound to the Ag presenting cell surface (T/F)

A

True

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12
Q

The TCR is always bound to the T cell surface and recognises Ag and MHC (T/F)

A

True

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13
Q

Antigen - define

A

a substance recognised by receptors of the adaptive immune system

Majority of antigens are proteins

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14
Q

How are antigens classified?

A

Can be classified via how they induce an immune response and their origins

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15
Q

Immunogen - define

A

Animmunogenis an antigen or any substance that may be specifically bound by components of the immune system (antibody, lymphocytes).

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16
Q

Haptens - define

An example of Haptens is viruses, what does this imply for the host immune response?

Hapten conversion to Immunogen - how?

Haptens introduced to mouse - outcome
Carrier protein introduced to mouse - outcome
Hapten + carrier protein introduced to mouse - outcome

Some antigens have low immune power, how is this combated?

Which factors influence antigen immunogenicity?  
A Foreignness of antigen; 
B Molecule weight of antigen
C Host's inheritance 
D Host's age
E Adjuvant
A

Haptens are small molecules that elicit an immune response only when attached to a large carrier such as a protein.

Since Haptens are too small to initiate an immune response, the body will not show any signs and symptoms

If a Hapten stays in the body for a long time, mutations can occur in the Hapten causing it to eventually bind to a carrier protein forming a hapten-carrier protein complex, which allows it to become Immunogenic since the size of the molecule is large.

Haptens introduced to mouse - No antibodies
Carrier protein introduced to mouse - Antibodies produced against carrier protein
Hapten + carrier protein introduced to mouse - Antibodies produced against haptens

Adding adjuvants to antigens can increase the immune response by increased attraction and uptake to APCs.

A, B, E

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17
Q

Diff between an antigen and a hapten

A

Anantigenis a complete molecule that can trigger an immune response by itself whereas
Ahaptenis an incomplete molecule that cannot trigger an immune response by itself.

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18
Q

Tolerogen - define

Foreign antigens/ Heteroantigens -
Self antigens/ Autoantigens -

1st, 2nd, 3rd lines of defense

State of unresponsiveness of immune system to antigens is?

State of unresponsiveness of immune system to self antigens is?

What happens if self tolerance fails?

How are immune responses to self antigens prevented in human body?

Tolerogen - define

What happens if the molecular form of tolerogen is changed?

Tolerogen - MoA

A

Tolerogen - A foreign antigen that suppresses immune response, or produces immune tolerance.

Heteroantigens - Not part of human body
Autoantigens - Body cells

1st line - skin + mucous membranes
2nd line - Inflammation, fever, innate immune cells
3rd line - T cells, B cells, APCs

Immune tolerance

Self tolerance

Autoimmunity (immune cells attack itself)

Antigen that invokes a specific non-responsiveness due to its molecular form.

If molecular form is changed, tolerogen can become an immunogen.

Instead of inducing the immune system to be active, the tolerogen binds to the antigen receptor of the lymphocytes in order to suppress it.

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19
Q

T lymphocytes are derived from

A

Haemopoietic stem cells in BM

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20
Q

T lymphocytes mature in

A

Thymus

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21
Q

T lymphocytes express TCRs on surface (T/F)

A

True

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22
Q

T lymphocytes does not require action of APCs to recognise specific Ag (T/F)

A

False; T lymphocytes require action of APCs to recognise specific Ag

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23
Q

How are T cells activated?

A

T cells are activated when they encounter antigenic peptide fragments bound to MHC molecules

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24
Q

What happens during and after T cell activation?

A
  • Ag-MHC complex activates TCR
  • T cell secretes cytokines
  • T cells differentiates into CD8+TC or CD4+TH cells
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25
Q

CD8+ T cells - main function

A

Primarily involved in destruction of cells infected by foreign entities

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26
Q

How are CD8+ T cells activated?

A

Activated by TCR interaction with peptide-bound MHC I molecules.
• Activated via Ag on APC and co-stimulatory signal or Ag on a nonAPC target cell and cytokines from CD4 T cells

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27
Q

Result of CD8+ T cell activation

A

• Clonal expansion – effector cells – utilize perforin, granzyme and granulysin

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28
Q

Most effector cells/mature T cells die – few retained as memory cells – subsequent infection (T/F)

A

True

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29
Q

Function of CD4+ T helper cell

A

Primarily involved in establishing and maximizing the
immune response
– Direct other cells to perform immune task

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30
Q

CD4+ T helper cell is activated by?

A

TCR interaction with peptide-bound MHC II

molecules

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31
Q

MHC I is found where?

A

nucleated body cells (not red blood cells)

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32
Q

MHC II is found where?

A

antigen presenting cells

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33
Q

Antigen is in MHC molecule (T/F)

A

True

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34
Q

T cells can recognize when antigen is on APC (T/F), if true what does it mean for CD4+ and CD8+ molecules?

A

T cell recognizes MHC II (CD4+)

T cell recognizes MHC I (CD8+)

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35
Q

BCR - antibody bound to membrane of B cell (T/F)

A

True

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36
Q

Antibody = soluble immunoglobulin (T/F)

A

True

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37
Q

Dendritic cells, B cells, Macrophages - professional APCs (Use MHC I) T/F

A

False; they use MHC II

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38
Q

Function of APCs

A

They present antigenic peptides

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39
Q

Why are professional APCs the molecules responsible for presenting antigenic peptides when when nucleated cells have MHC which is recognized by T cells?

A

Nearly all nucleated cells have MHC I. They have MHC I so they can present to a T cell.
Thus professional APCs are ones whose role is to present antigens.

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40
Q

How do antigens present in MHC molecule?

A

When virus enters cell, various processes in cells produce peptides, these peptides can present on cell surface. Antigen peptide moved to surface on MHC molecule.

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41
Q

Why would we want these nucleated cells to present to CD8 T cell?

A

Depends on where the antigens are found
i.e. location with respect to cell
Ag can be inside or outside cell
Pathogens inside cell:
Viruses - interested in nucleus where dna replication occurs
Bacteria - Brucella abortus, Listeria monocytogenes, Chlamydia trachomatis, Mycobacterium tuberculosis, Salmonella enterica - outside
T cell can’t enter cells
so MHC I is on cell surface so it can present antigens to the cytotoxic T cell whose main purpose is to kill cells.

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42
Q

Function of CD4+ T helper cell

A

Primarily involved in establishing and maximizing the
immune response
• Direct other cells to perform immune tasks

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43
Q

CD4+ T helper cell is activated by?

A

TCR interaction with peptide-bound MHC II

molecules

44
Q

Once T cell becomes activated, many events occur as a result, what are these events?

A

Can signal naive T cell to be activated
Can signal macrophage/ any other dendritic cells to be activated
Can signal B cells to mature to plasma cells
Can signal NK cells to beome activated and kill infected cells

45
Q

Two types of T cells - name them

A

CD8 cells - cytotoxic cells

CD4 cells - helper cells

46
Q

Activation of CD4 T cells is important for beginning of response in cell mediated immunity (T/F)
If true, what cells would be important to T cell activation?

A

True; APCs

47
Q

Types of APCs

A

Dendritic, macrophage, B cell (produces antibodies)

48
Q

Macrophages are a type of APC involved in T cell activation, how are MHCs involved with macrophages and T cells?

A

Macrophage engulfs bacteria, degrades into fragments and loads these fragments onto MHC II.
Then MHC II showcases the fragments to T cell.

49
Q

1st step of T cell activation - outline

A
  1. MHC II forms a complex with TCR – T cell can recognize the pathogen fragments on MHC II as non self
50
Q

2nd step of T cell activation - outline

A
  1. Costimulatory rxns required to confirm this binding of MHC II and TCR
    - B7 from macrophage and CD28 receptor on T cell interactions
    - CD40 from macrophage and CD40 ligand from T cell
    - CD4 from T cell will place the MHC II and TCR in the perfect orientation

Costimulation - enhancement of previous signal

51
Q

3rd step of T cell activation - outline

A
  1. Chemical signalling
    After these rxns macrophage releases chemicals
    i.e. IL-12. Receptors on T cell recognizes IL-12, genes will be transcribed and RNA translated
52
Q

4th step of T cell activation - outline

A
  1. IL-12 causes T cell to produce receptor on T cell surface called IL-2 receptor and T cell produces IL-2 which acts on ITSELF – known as autocrine signalling
53
Q

5th step of T cell activation - outline

A

Also produces Il-1 which converts naive T cells into helper T cells

Interferon gamma which acts on macrophage and signals to bring more macrophages to signal more T cells

54
Q

All immune responses have a call and response action so cells usually respond back to each other (T/F)

A

True

55
Q

Why do the T cells remain in the thymus for a bit?

A

T cells need to be trained in thymus then can go into circulation. From the T cells multiple cells will be produced.

56
Q

B cell class switching - define

A

Class switching is the process whereby an activated B cell changes its antibody production from IgM to either IgA, IgG, or IgE depending on the functional requirements.

57
Q

Effector B cells - define

A

Effector B cells are called plasma cells and secrete antibodies

58
Q

What does T cell activation cause in B cells?

A

Clonal expansion – effector cells – release cytokines –
activities including B cell class switching and affinity
maturation

59
Q

What is the fate of B cells after clonal expasion?

A

Most effector cells die – few retained as memory cells –

subsequent infection

60
Q

Types of CD4+ T helper cells

Why does the body need diff types of T helper cells?

A

• TH1
•– Intracellular/virus infection occurs. DCs/macrophages secrete IL-12 and present the peptide fragments to naive T cells in lymph node.
Once IL-12 signal is recognized, it stimulates naive T cell to become TH1.
The TH1 cell now:
- secretes interferon gamma (IFN-γ) which activates macrophages
- interferon gamma also stimulates production of antibodies that promote phagocytosis since they act as complement proteins (enhance phagocytosis by opsonization)
- also TH1 secretes IL-2 which stimulates growth and differentiation of T cells

• TH2
•– Parasitic infection occurs and APCs secrete IL-4, APC presents antigen to naive T cell which differentiates into TH2 cell.
TH2 Secretes:
IL-4 - stimulates B cells to produce IgE antibodies
IL-5 - activates mast cells and eosinophils
IL-13 - stimulates mucus production in intestines
Parasite too large for phagocytosis, MoA involves:
1. IgE antibodies coat parasite surface
2. Mast cells and eosinophils have receptors for Fc regions of the antibodies, so they bind to Fc region
3. Parasite killed by granule enzymes secreted by mast cells and eosinophils
4. Mucus secretions are to promote parasite expulsion from gut
– IgE producing B cells, mast cells and eosinophils

• TH17
•– Infection involving fungi and extracellular bacteria present. IL6 and transforming growth factor beta (TGF-beta) are produced by innate immune cells.
T cell recognizes antigens from pathogens presented on dendritic cell.
IL6 and TGF-beta induce tranformation of T cell into TH17
TH17 does the foll:
- Secretes IL17 which recruits neutrophils to infection site
- IL22 and IL17 stimulate epithelial cells to promote antimicrobial peptides that resist invasion
(Patients lacking gene for IL17 are more susceptible to bacterial and fungal infections)

• T-regs
Limit the tissue damage caused by immune response once a pathogen has been eradicated and suppress T cell response.
Prevents autoimmunity - communicate with other immune cells and help to stop their effector functions
Produces IL10 (suppress macrophage) and TGF-beta (induce generation of Treg cells) which help inhibit inflammation and immune response

• Follicular TH cells
•-- Involved in class switching and affinity maturation
- Produces IL-21 which guides B cells to make appropriate antibodies (class switching) to combat infection

Body encounters diff types of pathogens that infect diff parts of body and diff cells. E.g. helminths are too large to be phagocytosed and mycobacteria get ingested by phagocytes but resist phagocytosis. T helper cells will signal diff immune cells to help eliminate the pathogen.

61
Q

Intracellular pathogens - name

A

Mycobacteria, viruses , protozoa

62
Q

Initiators of response for intracellular pathogens - name

A

IL-12 secretion by Macs and DC, IFN-γ secretion by NK cells

63
Q

Responding T cell to initiators of response for intracellular pathogens\

A

TH1

64
Q

Clonal expansion - explain

A

In clonal selection, an antigen is presented to many circulating naive B and (via MHC) T cells,
and the lymphocytes that match the antigen are selected to form both memory and effector clones of themselves.

This mass production is termed “clonal expansion,” in which daughter cells proliferate into several generations of clones of the original parent cells.

65
Q 
Most effector cells die – few retained as memory cells –
subsequent infection (T/F)
A

True

66
Q

TH1 - role

A

• IFN-γ production; Ab production by B cells

67
Q

TH2 - role

A

• IL-4, IL-5, IL-13 production – IgE producing B cells, mast cells and eosinophils

68
Q

TH17 - role

A

• IL-17, IL-22 production – defense against Fungi and extracellular bacteria

69
Q

T-regs - role

A

• Limit/suppress Immune System – role in autoimmunity

70
Q

Follicular TH cells - role

A

• Involved in class switching and affinity maturation

71
Q

Types of CD4 Th cells

A

Th1, Th2, Th17, T-regs, Follicular Th cells

72
Q

Gamma delta (γδ) T cells - explain

A

Gamma delta (γδ) T cells are the prototype of ‘unconventional’ T cells and represent a relatively small subset of T cells in peripheral blood.

Gamma delta cells are lipid based so doesn’t need MHC I or II whilst alpha beta T cells are protein based

  • defined by expression of (TCRs) composed of γ and δ chains. This sets them apart from the classical and much better known CD4+ helper T cells and CD8+ cytotoxic T cells that express αβ TCRs.
  • Do not need APCs to function, can interact with all unbound antigens
  • Believed to be first line of defense, acting faster than alpha-beta T cells
73
Q

In the thymus, T cells diversify and undergo selection processes which are?

A

• Positive selection
• Permits survival of only those T cells which TCRs are
capable of recognising self-MHC molecules

  • Negative selection
  • Eliminates T cells that react too strongly with self-MHC or with self-MHC plus self peptides
74
Q

T cell

A

B and T lymphocytes arise from a common ancestral cell—lymphoid progenitor or common lymphoid precursor-2 (CLP-2). … During the development of T- and B-cell lines in the organs of the central immune system (thymus and bone marrow) they begin to express various cell surface markers.

75
Q

T cell lineage - Ontogeny

A

➢ Common lymphoid precursor leaves the bone marrow and migrates through the bloodstream
to the thymus.

—— Thymocytes early in development lack detectable CD4 and CD8, and are referred to as double-negative (DN) cells or T cell precursor. DN cells can become T cells, NK cell, Dendritic cell or B cell.

➢ These DN Pre-T cells differentiate into ɣδ DN Pre-T cells and ⍺β DN Pre-T cells.
ɣδ DN Pre-T cells leave the thymus to populate lymphoid tissue and epithelia.

➢ Most DN thymoctyes progress down the ⍺β developmental pathway.
They stop proliferating and begin to rearrange the TCR β-chain genes, then express the β chain.

➢ β chain combines with the pre-T ⍺ chain and the CD3 group to form the pre-TCR.

➢ The pre T cell advances to the double positive (DP) stage, as a Pro-T cell with the expression CD4 and CD8 correctors and the rearrangement of ⍺ chain genes to form the ⍺β TCR.

➢ DP thymocytes expressing ⍺β TCR-CD3 complex develop into immature CD4+ TH cells or CD8+ TC cells.

76
Q

What are HSCs?

A

Hematopoietic stem cells (HSCs) are the stem cells that give rise to other blood cells via haematopoiesis.

77
Q

B cells arise from?

A

HSC

78
Q

B cells roles

A 
• Can recognize free Ag directly
• Upon activation, undergo proliferation and
differentiation
• Plasma cells
      • produces Abs
      • undergo apoptosis once inciting agent is eliminated
• Memory B cells
• Major role in humoral immune responses
79
Q

Humoral immunity response to whole antigen in circulation

A
  1. Antigen –> engulfed by macrophage
  2. Fragments of antigen –> presents on macrophage and macrophages becomes APC
  3. APC –> activates Helper T cell
  4. Helper T cell can differentiate into B cell and cytotoxic T cell
80
Q

Humoral immunity response to free antigen/piece of antigen e.g. bacteria flagella

A
  1. Free antigen is recognized by B cells

2. B cells turn into plasma cells which produce antibodies

81
Q

Cell mediated immunity response to whole antigen inside normal cell

A
  1. Antigen is recognized by cytotoxic T cell

2. Cytotoxic T cell kills infected cells

82
Q

Humoral and cell mediated immunity response to whole antigen in circulation for the 1st time

A

Helper T cells and B cells would be changed to memory cells if infection is experienced for the first time since the immune sys will have to make memory cells
So we will have memory helper T cells and memory B cells.

83
Q

Abs bind to Ags, destruction occurring via ?

A
  • pathogen & toxin neutralization
  • Classical complement activation
  • Opsonisation promotion
84
Q

• Ag-Ab complexes are cleared by?

A

Complement cascade

85
Q

Properties of antibodies

A

Proteins that react specifically with the Ag that
stimulated their production.

Very specific, binding only on a particular Ag

Possess high affinity i.e. bind Ag very strongly

Are ~ 20% of plasma proteins

During electrophoresis, Abs are separated into the γzone – referred to as the gamma globulin fraction of
serum.

86
Q

What is primary function of Ag and what does this cause?

A

Primary function is to bind Ag

Can result in the inactivation of a pathogen
Opsonization (make pathogen more recognizable to immune cells)
Complement activation

87
Q

B cell activation process

A

An effective signal for B cell activation involves two distinct signals induced by membrane events
Occurs via two different pathways dependent on the nature of the Ag.
Antigens that can activate B cells in the absence of direct contact with TH cells are thymus independent (TI) antigens.
TI-1 Ags are mitogens - polyclonal B cell activators that are able to activate B cells regardless of the antigenic specificity e.g. LPS
TI-2 Ags activate by extensively cross-linking the mIg receptor and engaging several BCRs e.g. polymeric proteins - bacterial flagellin
Response to TI Ags is generally weaker, with no memory cells and a low level of class switching

88
Q

Diff btw T cell and B cell activation

A

T cell activation responsible for humoral and cell mediated immunity while B cell activation is responsible for cell mediated immunity.

89
Q

B cells role in antibody production

A

Can produce antibodies which are attached to B cell receptors

90
Q

Antibody variable region purpose

A

Variable region - rxn with antigen

91
Q

Somatic hypermutations in antibodies

A

Mutations occur in variable regions called somatic hypermutations. Since there are mutations the antibodies have diff variable regions so they can each bind to diff antigens.

92
Q

CD40 is present on surface of all APCs (T/F)

A

True

93
Q

Special T cells can identify B cells (T/F)

A

True

94
Q

An effective signal for B cell activation involves two distinct signals induced by membrane events (T/F)
Occurs via two different pathways dependent on the nature of the Ag. (T/F)

A

True

True

95
Q

Antigens that can activate B cells in the absence of direct contact with TH cells are

A

thymus independent (TI) antigens

96
Q

TI-1 Ags (Thymus independent antigens) are mitogens - define mitogen

A

polyclonal B cell activators that are able to

activate B cells regardless of the antigenic specificity e.g. LPS

97
Q

TI-2 Ags activate by B cells by?

A

extensively cross-linking the mIg receptor and

engaging several BCRs e.g. polymeric proteins - bacterial flagellin

98
Q

Response to TI Ags is generally (stronger/weaker?), with no memory cells and a (high/low?) level of class switching

A

Response to TI Ags is generally weaker, with no memory cells and a low level of class switching

99
Q

T independent antigens structure

A

Repeating structures that cross link the BCR or cross link PRRs and BCR

100
Q

T cells do not participate in response to T independent antigens, what does this mean for class switching?

A

No class switching will occur, only IgM will be produced

101
Q

Why can’t class switching occur for T independent antigen immune response?

A

CD40 ligand on T cell must interact with CD40 on B cell to induce class switching and T cells aren’t participating

102
Q

What will happen to the B cells without T cell assistance?

A

The B cells will proliferate into plasma cells which will secrete only IgM antibodies

103
Q

What will happen to the B cells without T cell assistance?

A

The B cells will proliferate into plasma cells which will secrete only IgM antibodies and some IgD

104
Q

TI-1 Ags (Thymus independent antigens) are mitogens - define mitogen

A

polyclonal B cell activators that are able to

activate B cells regardless of the antigenic specificity e.g. LPS

105
Q

TI-2 Ags activate by B cells by?

A

extensively cross-linking the mIg (membrane bound immunoglobulin) receptor and engaging several BCRs e.g. polymeric proteins - bacterial flagellin

106
Q

Are host cells recognized by the innate or adaptive immune system?

A

No, however host cells can express substances on receptors such that when immune system cells bind their phagocytic actions are inhibited

Immunology (4 decks)

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