Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Immunology > Basic immunology > Flashcards

Basic immunology Flashcards

1
Q

What are the two divisions of the immune system?

A

Adaptive and inate immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the main components of the innate immune system?

A

Epithelial barriers
Phagocytes/dendritic cells
Complement
NK cells and innate lymphoid cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are teh two main components of the adaptive immune system?

A

Humoral immunity (antibody mediated)
Cell mediated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Comparing the innate and adaptive immune system:
Describe the kinetics of the innate and adaptive immune system?

A

Innate - hours to days
Adaptive - days to weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Comparing the innate and adaptive immune system:
Describe the specificity of the innate and adaptive immune system?

A

Innate - limited specificity ie able to recognize groups of related microbes etc

Adaptive - Highly specific for individual antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Comparing the innate and adaptive immune system:
Describe the memory of the innate and adaptive immune system?

A

Innate - nil memory

Adaptive - Memory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the main receptor implicated in the innate immune system? What can these receptors recognise?

A

Pattern recognition receptors
- these are able to recognise pathogen associated molecular patterns (PAMPs) OR patterns of molecules release by stressed or dying cells (Danger associated molecular patterns aka DAMPs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Are pattern recognition receptor on the innate immune system germline or somatic?

A

They are germline and invariant (ie dont change throughout the immune respone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Pattern recognition receptors of the innate immune system can be either cell surface associated or soluble. What are the two main cell surface related pattern recognition receptors?

A

Toll like receptors (TLRs)
- found on the plasma surface OR on the endosomal surface in most cells of the immune system
- labelled 1 through 9

Nod like receptors (NLRs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Deficiency in which Toll like receptor results in a susceptibility to HSV encephalitis?

A

TLR3
- receptor to dsDNA, therefore if dont have it then susceptible to dsDNA viruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are some soluble receptors of the innate immune system? (list 3)

A

Pentraxins (example: CRP)
Collectins
Complement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the cellular components of the innate immune system?

A

Epithelial barriers
Phagocytes
Dendritic cells
NK cells
Innate lymphoid cells
Mast cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Many cells are capable of phagocytosis. What are the two main types of “professional” phagocytes in the innate immune system?

A

Neutrophils
Monocytes/macrophages

Tissue dendritic cells are also somewhat professional phagocytes, but their main purpose in to be an antigen presenting cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the difference between monocytes and macrophages?

A

Macrophages are monocytes when they are in the peripheral tissues

Monocytes are found in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is chronic granulomatous disease? Briefly explain the genetics, pathophys, presentation, treatment

A

This is a neutrophil function disorder

It is X linked, autosomal recessive
Usually male pts (due to X linked), usually in infancy

It is due to CYBB gene defect leading to GP91phox deficiency. This results in failure of the respiratory burst which is required to form ROS needed to kill phagocytosed pathogens

Presents with recurrent severe bacterial and/or fungal infections
These are very unwell pts at presentation

Have inflammatory granulomata esp in GIT

Treatment if BMT and ab prophylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are NK cells? What is their role?

A

They are an innate lymphopid cell part of the innate immune system

Major function is to kill infected cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the adaptive immune system counter part of NK cells?

A

cytotoxic CD8 T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do NK cells kill infected cells?

A

NK cells have activate receptor and inhibitory receptor on cell surface
The balance between the intensity of the activation vs inhibitory signal when the NK cell handshakes with another cell determines whether it is activated or not

For example, down regulation of MHC1 in viral infected cell results in loss of inhibitory signal that results in activation of NK cell leading to death of the viraly infected cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the three effector functions of NK cells?

A

Recognise cells with markers of infection or stress
-> exocytose granules containing perforin, granzyme leading to cell death

Recognise cells coated in antibody
-> participate in antibody dependant cell mediated cytotoxicity

Secrete cytokines to amplify immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the main clinical correlate of NK cell dysfunction?

A

Haemophagicytic lyumphohistiocytosis (HLH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is haemophagocytic Lymphohistiocytosis (HLH)? Explain the causes of primary vs secondary HLH

A

It is a primary or secondary loss of function of NK cells and cytotoxic T lymphocytes (CD8 T cells)

Primary - due to gene defect eg perforin gene
Secondary - malignancy, autoimmunity, infection (eg EBV, HIB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Explain the pathophysiology of HLH?

A

Failure of cytotoxicity
this leads to a positive feedback system and progressive immune activation. Progresses to cytokine storm and uncontrolled inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Where are dendritic cells found?

A

Constitutionally present in epithilia and most tissues of the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the main role of dendritic cells?

A

professional antigen presenting cell part of the innate immune system
Links the innate and adaptive immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

There is a specific type of dendritic cell that is highly relevant in the antiviral response. What is it and how is it implicated in the antiviral response?

A

Plasmacytoid dendritic cell
produces type 1 interferon which is involved in the antiviral response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is complement?

A

It is a part of the innate immune system
It is a range of serum proteins that perform a variety of roles in the immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Why are there so many steps in complement activation?

A

the numerous components and steps in complement activates reflects the need to tightly control the activation due to potential damage if uncontrolled activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the three effector functions of complement?

A

Complement fragments released by cascade opsonise (coat) microbes that are then recognised by phagocytes

Results in the release of anaphylatoxins (C3a, C5a) which stimulates inflammation

Results in the formation of the membrane attack complex (MAC) by the terminal pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the three pathways of complement activation?

A

Classical (antibody mediated)
Lectin (antibody independent)
Alternative (antibody independent)

30
Q

Explain the complement classical pathway?

A
  • C1(q) binds to antibody stuck to antigen
  • r and s components of C1 cleave C4 into C4a and C4b
  • C4b cleaves C2 into C2a and C2b
  • C4b and C2b remain bound. C4bC2b = classical C3 convertase (conversion point of the three pathways)
  • C3 convertase (C4bC2b) cleaves C3 into C3b and C3a
    -> C3a is an anaphylatroxin
  • C3b remains bound to C4aC2b forming C4aC2bC3b (C5 convertase complex)
  • C5 convertase cleaves C5 -> terminal complement pathway and MAC
31
Q

Explain the alternative complement pathway?

A

C3 spontaneously can split into C3a and C3b in the blood (known as C3 tickover)
- If there is nil pathogen around, the free C3b will be inactivated, however if there is a pathogen C3b with stick to the pathogens surface
- Surface bound C3b binds to factor B
- Free factor D then cleaves the bound factor B into Bb and Ba
- C3bBb complex = C3 converter complex
- The alternative C3 convertase complex performs same role as the classical C3 convertase complex
-> it forms the alternative C5 converstase complex (C3bBbC3b)

32
Q

Explain the lectin complement pathway?

A

Basically the same as the classical pathway except it is initiated by Manose binding lectin that binds to manose residues on the cell surface of micro-organisms and cleave C4

33
Q

Explain the terminal pathway?

A

C6, C7, C8 bind together with C5b
This complex results in the insertion of multiple C9 (poly C9) through the cell membrane (MAC)
- this results in cell death

34
Q

What do early classical pathway complement deficiencies typically result in?

A

SLE predispoosition
Minimal increased risk of infection EXCEPT with C1q deficiency (encapsulated organisms)

35
Q

What does C3 deficiency typically result in?

A

SLE predispoosition
Membranoproliferative GN predisposition
Pyogenic bacterial infections (Gram neg > gram pos)

36
Q

What do deficiency in C5-9 result in?

A

susceptibility to neiseria

37
Q

What are the 2 main complement studies and what do they assess?

A

CH50 (aka CH100)
- tests to total complement pathway (ie classical, alternative and lectin) EXCEPT ealry alternative pathway (Factor B, factor D, properdin)

AH50 (aka AH100)
- tests the alternative pathway

38
Q

Which test (CH50 or AH50) is performed initially?

A

start with CH50, then perform AH50.

Together these results can indicate the specific part of the complement system that is affected

39
Q

What does CH50 and AH50 normal mean?

A

normal, nil complement issues

40
Q

What does CH50 normal, AH50 low mean?

A

Problem with early alternate pathway eg Factor B, D properdin)
- the only part the the CH50 doesn’t detect but the AH50 will

41
Q

What does CH50 low, AH50 normal mean?

A

Problem with early classical pathway
- C4 low = C4 def
- C4 normal = C1q or C2 def

42
Q

What does CH50 low, AH50 low mean?

A

Problem with common pathway (ie C3 or terminal pathway)
- C3 low = C3 def
- C3 normal = C5-9 def

43
Q

What are type 1 interferons? What are the most common examples of type 1 interferons?

A

Large family of structurally related proteins that mediate the early innate immune response to vial infections

Examples: INF alpha, INF beta

44
Q

How is type 1 interferon production stimulated?

A

Most potent stimulus is viral nucleic acids
Activates or PRRs of the innate immune system (ie by viral nucleic acids) stimulation Type 1 IFN gene expression in many different cells

45
Q

Where are teh receptors for Type 1 IFN loacted? what is teh effect of stimulation of these receptors?

A

receptors for IFNs (IFNART1/2) are located on all nucleated cells in the body
- stimulation of these receptors leads to signals to activate transcription factors that leads to protein production that protects against viral infection

46
Q

What is a recently development in our understanding of IFN in relation to severe covid infection?

A

Recently discovered that many elderly pts with severe covid 19 infection actually have antibodies against type 1 interferon (ie dampens their anti viral response)

Also implicated in pts who get west nile virus encephalitis

47
Q

What are the main cellular components of the adaptive immune system?

A

Antigen presenting cells (dendritic cells)
B lymphocytes
T Lymphocytes

48
Q

What are the three types of T cells and their function (briefly)?

A

CD4 T helper cells - stimulate proliferation and differentiation of T lymphocytes and active other cells includeing B cells

CD8 cytotoxic T cells - Kill infected/ tumor cells

T ref cells - inhibit and control the immune response

49
Q

Briefly describe B cell development?

A

Common lymphoid progenitor cell
-> pro B cell -> Pre B cell -> immature B cell

This immature B cell is then released into the periphery (blood) as a mature (naive) B cell

It can encounter an antigen in the periphery or germinal centre of LN. Once an antigen is encountered it is no longer naive

Then can develop into plasma cell or memory B cell

50
Q

Briefly describe T cell development?

A

In the thymus, pre T cell becoimes double positive T cell (CD4 and CD8)
- then either becomes CD8 OR CD4 T cell (immature at this stage)
- These imature CD4 or CD8 T cells then released into periphery as mature T cells

CD4 T cells further develop into various types

51
Q

What are the components of a B cell receptor / antibody?

A

2x light chains kappa or lambda
2x heavy chains (IgG, IgM, etc)

52
Q

Is VDJ recombination somatic or germline?

A

It is Somatic

53
Q

What is VDJ recombination?

A

this is the process or rearrangement to generate diversity in B and T cell receptors
Occurs whilst B and T cells are developing, BEFORE these cells met an antigen

54
Q

Where does VDJ recombination occur?
Where does VJ recombination occur?

A

VDJ recombination
- Ig heavy chain
- TCR beta and delta chains

VJ recombination
- Ig light chain
- TCR alpha and gamma

55
Q

Where is MHC1 found? Where is MHC2 found?

A

MHC1 - present on all nucleated cells + platlets
- absent from RBCs

MHC2 - present on professional APCs (macrophages, B cells, Dendritic cells)

56
Q

What is the role of MHC1 vs MHC2?

A

MHC1 presents antigens to CD8 T cells to allow CD8 T cells to directly kill vcirally infected cells

MHC2 presents peptides to CD4 T cells to shape the adpative immune system

57
Q

Explain T dependent B cells response briefly?

A

B cells migrate through peripheries and peripheral lymphoid tissues and can pick up soluble antigens
- these B cells then migrate towards the lymph node paracortex where the T cells are located

APCs present antigen to CD4 T cells in the paracortical region of the lymph nodes

B and T cells specific for teh same antigen meet in this area
- B cell presents antigen to T cell.
- T cell then sends signal to B cell to activate it

58
Q

Explain the molecular handshake between T and B cells during T dependent B cell response?

A

T cell receptor binds to antigen bound to B cell receptor
Co-stimulatory signal from CD40 ligand on T cell binding to CD40 on B cell

This handshake results in T cell producing cytokines that result in B cell differentiation

59
Q

What is antibody class switching recombinaiton? How doses this occur

A

Antibody class switching is the process leading to a change in the Ig isotype of an antibody produced by a activated B cell

B cells receptors are basically IgM stuck to the surface
therefore initial Ig produced in infection is IgM
Class switching recombination is responsible for a change from IgM to other isotypes

it occurs by cutting and rearanging the heavy chain

60
Q

Why dose class switching recombination occur?

A

Different types of Ig are good at dealing with different kinds of infections

61
Q

What two key B cell events occurs in the germinal center? What is the purpose of these events?

A

Somatic hypermutation
Affinity maturation

this is the process or lots of point mutations with the aim of producing B cells with the highest possible affinity for a specific antigen. Newly created B cells with high affinity are selected to survive (affinity maturation)

62
Q

What is hyper IgM syndrome? explain the genetics, pathophys, presentation and treatment?

A

Hyper IgM syndrome is X linked, males usually affected

Pathophys: Usually def in CD40L on T cells resulting in failure of co-stimulation of B cells by the CD4 T cell resulting in primative immune response (only IgM made)

Presents in unwell in infancy with recurrant sinopulmonary infection esp encapsulated organisms

Pts with have normal or high IgM, low other Ig

Treat with IVIG, Ab prophylaxis

63
Q

What are the subclasses of IgG?

A

IgG1-4

64
Q

What are the main Ig isotypes / subclasses that fix complement?

A

IgM, IgG1, IgG3

65
Q

Explain T cell activation? Explain the T cell activation handshake (activation and inhibition)?

A

T cell activation occurs when APC presents antigen to T cell
- T cell receptor binds antigen on MHC2 of APC
- Costimulatory molecules (CD80/86) on APC bind to CD28 on T cell completing the handshake
-> if pathogen is present, there will be up regulation of CD80/86 on APC which allows it to bind to the relativly low affinity CD28 on T cell -> activation
-> if antigen not present then CD80/86 will not be very present, so will only bind to the higher affinity CTLA 4 on T cells which is a inhibitory signal for T cell

66
Q

What are the four main types of CD4 T cell to know about? What is the cytokine associated with each of these subtypes?

A

Th1
- IFN gamma, IL2

Th2
- IL4, IL13

Th17
- IL17a, IL22

Treg
- IL10, TGF beta

67
Q

What is XLA (X linked agammaglobulinaemia)?

A

X link monogenetic primary immunodeficiency
- Due to defect in Btk enzyme, resulting in failure of B cell maturation in the bone marrow -> no Ig able to be made

Presents in males at 6-9 months, unwell

68
Q

At what ages do primary immunodeficiencies typically become apparent? why this age?

A

6-9 months
This is because maternal IgG lasts until 6-9 months

69
Q

What is SCID (severe combined immunodeficiency)?

A

X link monogenetic primary immunodeficiency resulting in inability to form T or B cells

70
Q

What is CVID (combined variable immunodeficiency)?

A

Characterized by recurrent infections and low antibody levels, specifically in immunoglobulin (Ig) types IgG, IgM, and IgA

Immunology (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions