Brainscape's Knowledge GenomeTM

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


See full index

PART ONE REVISION. > IMMUNOLOGY - Basic (B-cells/T-cells, Immunoglobulins, MHC) > Flashcards

IMMUNOLOGY - Basic (B-cells/T-cells, Immunoglobulins, MHC) Flashcards

1
Q

Which immunoglobulin passes through the placenta to assist foetal immunity?

A

IgG

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

What is the main immunoglobulin in human tears?

A

IgA

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

What receptors do macrophages have? (3)

A
  1. pattern recognition receptors which recognise microbial components
  2. surface receptors that recognise Fc portion of immunoglobulin and complement components. Binding of these receptors to their ligands enhances phagocytosis of antigen (opsonisation)
  3. MHC class II molecules on surface when activated - present antigen to helper T-cells. Secrete IL-12 which directs T-cell differentiation to Th1 subset.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What pro-inflammatory cytokines do macrophages produce?

A

IL-1, IL-6, and TNF

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

Which complements are involved in the terminal pathway (membrane attack complex) and its deficiency predisposes to Neisserial infections?

A

C5-C9 (C3 is also associated)

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

IL-2 is produced by what cells?

A

CD4+ cell

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

HLA Class I Antigens vs
HLA Class II Antigens

A

Class I : all nucleated cells, allows CD8+ cytotoxic T cells to recognise and eliminate virus infected cells

Class II: macrophages, dendritic cells, B cells, endothelial cells, allows initiation of immune response by interaction with T-helper CD4+ cells

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

difference in structure between class 1 and class II HLA

A

picture

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

What cytokines do TH1 produce?
What cytokines do TH2 produce?

A
  1. TH1 : IFN-gamma, IL2 –> B cells, NK cell and macrophage activation
  2. TH2: IL3, IL4, IL5, IL6 –> mast cell and eosinophil activation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the main functions of interferon? (3)

A
  1. activation of NK cells and macrophages
  2. directive antiproliferative action on tumour and virus infected cells
  3. increased expression of Class 1 HLA on infected/tumour cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What cells produce interferon?

A

T lymphocytes & macrophages

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

Which immunoglobulin is the first antibody to appear in infection?

A

IgM

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

What pathway does IgA activate?

A

Activates the alternative complement pathway (unlike other antibodies that activate the classical pathway)

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

What are the main types of eicosanoids? (3)

A
  1. Prostaglandins
  2. Leukotrienes
  3. Thromboxanes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the role of thromboxanes? (3)

vs

What is the role of leukotrienes? (3)

A

thromboxanes:
vasoconstriction, platelet aggregation and bronchoconstriction

leukotrienes
Bronchoconstriction, vasocontriction and increased vascular permeability

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

What is the cyclo=oxygenase pathway?

A

See diagram.

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

What is the effect of prostaglandin I2?

A

causes vasodilation and reduced platelet adhesion

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

What are the effects of prostaglandin E2? (5)

A
  1. vasodilation
  2. bronchodilation
  3. Release of pituitary hormones, adrenal cortex steroids and insulin from pancreas
  4. Macrophage activation
  5. Uterine contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are antigens? Definition

A

molecules (sugars, proteins or glycoproteins) that are immunogenic (cause immune cell proliferation) and reactive (cause production of antibodies)

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

What are the main secretion chemicals from mast cells? (3)

What is their main function?

A

histamines, leukotrienes and prostaglandins

  1. They work on plasma endothelial cells to cause p-selectin protein translocation to the cell surface –> monocyte/neutrophil margination/activation into interstitial space.
  2. endothelial cell contraction which creates spaces between endothelial cells which allows plasma leakage through the pores into interstitial place to cause swelling/oedema (INCREASED VASCULAR PERMEABILITY)
  3. Nociceptor activation to cause pain (usually by bradykinins)
  4. smooth muscle relaxation –> vasodilation (localised hyperaemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the function of phospholipase A2?

A

breaks down phospholipids into arachidonic acid

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

What do macrophages secrete?

A
  1. IL-1 and TNF-alpha –> activates plasma endothelial cells cause selectins to translocate to endothelial cell surface to cause monocyte and neutrophil activation.
  2. IL-8 binds to receptor on endothelial surface cell membrane –> ICAM/VCAM proteins on cell surface membrane –> monocyte/neutrophil activation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the effects of IL-1 and TNF-alpha? (4)

A
  1. activates plasma endothelial cells cause selectins to translocate to endothelial cell surface to cause monocyte and neutrophil activation.
  2. activates hypothalamus to secrete PGE2 which initiates fever –> denaturation of pathogen proteins and increase metabolism.
  3. acts on liver to produce acute phase reactant proteins (CRP - also activated by IL-6)
  4. acts on bone marrow to increase leukocytosis.
24
Q

What is the main difference between macrophage and neutrophil in terms of breakdown of pathogen process?

A

macrophage is APC cell so exposes antigens with MHC2 to cell surface

neutrophils breaks down and exocytosis the antigen. They also release NETS (chromatin) which attach to foreign microbes which are broken down by cathepsin G.

25
Q

Where are complement proteins synthesised?

A

In the liver

26
Q

What is the lysis mechanism of classical complement pathway?

A

antibodies (IgG) attach to antigens of PATHOGEN, exposing Fc portion to complement proteins

C1 attaches to Fc portion –> forms complement cascade complex in form of C1 + C4 + C2 +C3a/C3b + C5a/5b + C6 + C7 _ C8 + C9.

C3a/C5a - breaks off and is chemotaxic agent
for more WBCs to enhance inflammatory response

C5b/C6/C7/C8/C9 breaks off complement complex, forms a membrane attack complex (MAC) on cell surface of pathogen, creating a channel to allow water and Na+ influx into the pathogen, which eventually causes lysis of pathogen.

27
Q

What is the mechanism of opsonisation part of the classical complement pathway?

A

C3b of complement after chemotaxis by C3a recruits macrophages/neutrophils (more often macrophages) has C3b receptor of macrophages to encourage phagocytosis of whole pathogen and complement protein complex.

OPSONISATION –> enhancement of phagocytosis

28
Q

What are the 3 main mechanisms of complement pathway?

A
  1. Membrane attack complex
  2. Opsonisation
  3. C3a + c5a (chemotaxis)
29
Q

What is the alternative complement pathway?

A

direct access of complement C3b to directly attach to antigen on pathogen (without antibody).

C3b releases c3a to enhance macrophage recruitment

C3b then attaches to C5b –> C6 + C7 + C8 + C9 which then breaks off to form membrane attack complex on the pathogen surface which encourages H2o and Na+ influx which causes lysis.

30
Q

What is the mechanism of the lectin pathway?

A

mannose-binding lectin acts on the antigen on pathogen and recruits C4.

C4 –> C2 –> C3b –> C5b –> C6 –> C7 –> C8 –> C9.

1) Opsonisation - C3b is an opsinin so recruits macrophage as it has C3b receptor –> phagocytosis by macrophage or exocytosis by neutrophil

2) Membrane attack complex - C5b -> C9 come off and form MAC which attaches onto pathogen surface and encourages lysis

3) Chemotaxis by C3a and C5a

31
Q

What are the different types of interferons?

A

alpha, beta and gamma

alpha and beta - grouped together and produced by tissue cells

gamma - usually produced by immune cells.

32
Q

What is the mechanism of activation of interferon alpha and beta?

what are their effects?

A
  1. host cell infected with virus
  2. IRF transcription factor activated to produce interferons alpha and beta
  3. alpha and beta interferons released into plasma/system

EFFECTS
1. alert nearby tissues/healthy cells to stimulate production of protein kinase R (anti-viral peptides) to destroy virus
2. activates natural killer cells to initiate apoptosis of infected host cells

33
Q

What is the structure of a toll-like receptor? Are they part of the adaptive or innate immune system?

A

single membrane-spanning non-catalytic receptors

Part of the adaptive immune system.

34
Q

Which is the most abundant antibody? Where are they prodimantly located.

A

IgG, 65-70% in the blood plasma and produced by plasma cells.

35
Q

What are the primary mechanisms of IgG?

A

Secreted much more in the secondary immune response.

  1. Initiate complement cascade which enhances opsonization and MAC

2.neutralises viral proteins on their surface preventing their binding and infection of host cells

  1. binds to free antigen to trigger precipitation (antigen/antibody complexes) to trigger opsonisation and phagocytosis
  2. placental production of IgG to encourage passive immunity for baby
36
Q

What is the structure of IgA antibody vs IgG antibody?

A

IgA - dimer
IgG - monomer

37
Q

Where is IgA primarily located? (4)

A
  1. Sweat
  2. Saliva
  3. Mucosal lining of GI tract
  4. Milk (lactation)
38
Q

What is the structure of IgM antibodies?

A

Pentamer or monomeric.

39
Q

Where are IgM antibodies primarily located and which mechanisms do they activate?

A

Blood, lymph and some mucosal surfaces –> does not readily enter tissues from bloodstream due to its larger size.

Usually made during primary immune response (first exposure to certain antigen)

Usually activate complement proteins –> MAC + opsonisation

Involved in agglutination reactions (mismatch blood tranfusion) and involved in type 2 hypersensitivity reactions.

Can also be a B-cell receptor.

40
Q

Where are Type IgE antibodies primarily located? (3)

A
  1. respiratory tract mucosa
  2. urogenital structure
  3. lamina propia/lymphatic tissues.
41
Q

What is the structure of IgE antibodies?

A

monomer

42
Q

Which type of sensitivities can IgE cause? Which cell does it activate?

A

Type I hypersensitivity - anaphylaxis.

Activates mast cells (FcER1 receptor) to cause production of histamines, prostaglandins and leukotrienes. Increases vasodilation and vessels become leaky which increase interstitial oedema and constrict bronchi.

Activates eosinophils against parasites

43
Q

What is the structure of IgD antibodies?

A

monomer

44
Q

What is the function of IgD antibody?

A

Main B-cell receptor.
IgM can also be a B-cell receptor.

45
Q

What is the difference between passive and adaptive immunity?

A

PASSIVE: acquired from mother (IgG and IgA)

ACTIVE: actually getting infection from pathogen or from vaccines as they initiate antibody type response.host

46
Q

How are precursor T-cells from bone marrow translocated to the thymus?

A

Chemotaxic agents from thymus are released: thymosin, thymotaxin, thymopoetin and thymic factors.

47
Q

How does the precursor T cell develop?

A

Thymosin, thymopoetin, thymic factors stimulate RAG1 and RAG2 proteins to produce T-cell receptors which translocate to cell surface.

CD4/CD8 T cells then translocate to cell surface. These CD4/CD8 bind with MHC-II and MHC-I receptors respectively on thymic endothelial cells.

CD4 / MH2 predominant –> T helper cell

CD8 / MH1 predominant –> Cytotoxic cell

DUe to CD25/IL2 these T-helper/cytotoxic t cells can become regulatory t-cells to prevent autoimmune disease –> regulatory t cells located in the hassal’s corpuscles of thymus gland.

these cells can be sent to secondary lymphoid tissue (spleen, lymph nodes etc).

48
Q

What is the derivative of macrophages?

A

monocytes

49
Q

What hypersensitivity reactions are macrophages involved in?

A

Type 4 hypersensitivity reactions

50
Q

Exotoxins are released by which bacteria?

A

Gram positive bacteria

51
Q

Which immunoglobulins can activate the classic complement pathway?

Which immunoglobulins can activate the alternative complement pathway?

A

Classic: IgM, IgG1, IgG2, IgG3
Alternative: IgA, LPS, techoic acid, dextran,

52
Q

Make this into cards.

A

All immunoglobulins consist of 4 polypeptide chains - 2 identical heavy chains bound to 2 identical light chains. Each light chain consists of a varible domain (the amino acid sequence varies among light chains of different antibodies) and a constant domain. There are two types of light chains - lambda and kappa chains. No functional differences have been found between antibodies composed of lambda or kappa light chains. Each heavy chain consists of one variable domain and a number of constant domains - IgM and IgE have 4 heavy chain constant domains, whereas IgG, IgD and IgA have 3 heavy chain constant domains. The variable domains of both the heavy and the light chains combine to form the antigen-binding site, and confer specificity on the antibody. The unique sequence of the variable regions of the antigen-binding site of individual antibody molecules is termed the idiotype. The heavy chain constant region of different antibodies differs in structure, and it is this portion of the antibody that determines the class (isotype) and thus its different properties and effector functions. There are five immunoglobulin isotypes in humans- IgG, IgM, IgA, IgE and IgD. Antibodies bind to conformational epitopes i.e., sites on the antigen surface brought together by folding - they recognise tertiary and quarternary structures of proteins and carbohydrates. Some antibodies recognise and bind to linear segments of polypeptide. The enormous antibody repertoire in humans is mostly the result of combinatorial rearrangement of germline immunoglobulin genes encoding the variable regions of the heavy and light chains.

Immunoglobulin genes coding for heavy and light chains are located on different chromosomes. The genes encoding the heavy chain are found on chromosome 14 in humans. Genes encoding the kappa light chain are found on chromosome 2 and the human lambda light chain gene cluster is located on chromosome 22.

53
Q

What is the order of half-life of the immunoglobulins from longest to shortest?

A

IgG - 21 days
IgA - 7 days
IgM - 5 days
IgD - 3 days
IgE - 2 days

54
Q

Hypogammaglobulinaemia has which immunoglobulin deficiency?
Which bacteria is it most susceptible to?

A

IgG deficiency
Susepticibility to encapsulated organisms (staphylococcus, strep pneumoniae, Group B strep, Klebsiella, Haem type B)

55
Q

THe Fc region of immunoglobulins is binding site for (3)

A
  1. mast cells
  2. transplacental transfer properties
  3. activation of complement cascade
56
Q

Make cards of this:

A

Interferons are cytokines. There are three types of interferons - IFN-alpha is produced primarily by mononuclear phagocytes, INF-beta is produced by fibroblasts and interferon-gamma is produced by T cells and NK cells. IFN-alpha and IFN-beta are termed type I interferons. The type I interferons bind to the same cell surface receptor.

The interferons are anti-viral proteins produced by cells in response to viral infection. Their functions include:
inhibition of protein synthesis and DNA replication in virus-infected cells
increase in MHC class I expression and antigen presentation in all cells
activation of NK cells to kill virus-infected cells.

Interferon alpha has been shown to inhibit cell proliferation in vitro. This cytokine is an endogenous pyrogen and is one of the causes of fever and myalgia in infection. Indications for alpha-IFN therapy include hairy cell leukemia (90% response rate), renal cell carcinoma, chronic active hepatitis B or C, juvenile laryngeal papillomatosis (HPV induced) and Kaposi’s sarcoma in AIDS.

Gamma-IFN acts as an immune regulator and augments phagocytic activity; it has its own receptor. It is used clinically in patients with chronic granulomatous disease, although its precise mechanism of action is unclear. It may increase production of superoxide ion in neutrophils in these patients.

IFN-beta is used in the treatment of patients with multiple sclerosis.

57
Q
A

PART ONE REVISION. (80 decks)

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