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Pathology > Immunology > Flashcards

Immunology Flashcards

1
Q

What are the two types of immunity

A
  1. Innate (non-specific)

2. Adaptive (specific)

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2
Q

Describe the cellular contributors to innate immunity

A
  • Phagocytic cells

- Natural killer cells (non-MHC-restricted killing)

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3
Q

What mediates adaptive immunity

A
  • Lymphocytes

- Antibodies

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4
Q

Define an antigen

A
  • Any substance capable of producing an immune response

- A substance binding specifically to an antibody or T-cell antigen receptor

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5
Q

What are the two ways the body can respond to an antigen

A
  1. Cell-mediated immunity

2. Humoral immunity

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6
Q

What cell does cell-mediated immunity respond to

A

T-lymphocytes

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7
Q

What cell does humoral immunity respond to

A

Immunoglobulins produced by plasma cells derived from B-lymphocytes

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8
Q

What are the light immunoglobulin chains

A
  • Kappa

- Lambda

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9
Q

Define opsonisation

A

The coating of a surface of a foreign material by complement to promote engulfment by phagocytic cells which have cell-surface receptors for complement

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10
Q

List the 5 classes of immunoglobulin

A
  • IgG
  • IgM
  • IgA
  • IgD
  • IgE
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11
Q

What creates diversity among antibodies

A

Variability of the amino acid sequences in the N-terminal regions

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12
Q

What are the two main types of T-lymphocytes

A
  1. Helper T-cells (CD4+)

2. Cytotoxic T-cells (CD8+)

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13
Q

What is the role of helper T-cells

A

Respond to antigenic stimulus by producing cytokines, which activate T-cells, B-cells, and macrophages

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14
Q

What is the role of Major Histocompatibility Complex (MHCs) Antigens

A

Present antigenic peptides to T-cells

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15
Q

What diseases are associated with the HLA-DR3 subtype

A
  • Addison’s
  • Hashimoto’s
  • Myasthenia gravis
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16
Q

What diseases are associated with the HLA-DR4 subtype

A

IDDM

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17
Q

Where do all lymphoid cells originate

A

Pluripotential stem cells of the bone marrow

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18
Q

Where do lymphoid progenitor cells destined to become T-cells migrate to

A

Thymus

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19
Q

Where does B-cell development occur

A

Bone marrow

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20
Q

List the secondary lymphoid organs

A
  • Lymph nodes
  • Spleen
  • MALT
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21
Q

Describe the cortical structure of lymph nodes

A

Primary follicles of B-lymphocytes surrounded by T-cells of the paracortex

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22
Q

Where is the lymphoid tissue of the spleen situated

A

Within the white pulp

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23
Q

List the 3 areas of MALT (mucosa-associated lymphoid tissue) in the gut

A
  • Peyer’s patches (terminal ileum)
  • Lamina propria cells
  • Intraepithelial cells
24
Q

What cells can be antigen-presenting cells (APCs)

A
  • Dendritic cells
  • Macrophages
  • B-cells
25
Q

What must antigens be presented alongside to be recognised by T-cells

A

MHC class 2 antigen

26
Q

What activates the ‘classical’ complement pathway

A

Antigen-antibody (immunoglobulin) complexes

27
Q

What activates the ‘alternative’ complement pathway

A

Bacterial cell surfaces

28
Q

What is the outcome of both complement pathways

A

Production of membrane attack complexes

29
Q

List the functions of complement

A
  • Bacterial killing or target cell killing by membrane lysis
  • Opsonisation promoting phagocytosis
  • Removal of immune complexes
  • Mediation of vascular and cellular components of acute inflammation
30
Q

How can immune deficiency be classified

A
  • Specific deficiencies

- Non-specific deficiencies

31
Q

How are specific immune deficiencies divided

A
  1. Primary = due to an intrinsic defect in the immune system (usually genetic)
  2. Secondary = due to an underlying condition
32
Q

Define type 1 hypersensitivity

A

Immediate hypersensitivity due to overproduction of IgE on mast cells of basophils

33
Q

Examples of type 1 hypersensitivity

A
  • Asthma
  • Hayfever
  • Allergic rhinitis
34
Q

Define type 2 hypersensitivity

A

Cytotoxic - antibody to cell-bound antigen

35
Q

Examples of type 2 hypersensitivity

A
  • Transfusion reactions
  • Rhesus incompatibility
  • Autoimmune haemolytic disease
  • ITP
  • Myasthenia gravis
  • Goodpasture’s syndrome
36
Q

Define type 3 hypersensitivity

A

Deposition of immune complexes in the tissues

37
Q

Pathophysiology of type 3 hypersensitivity

A

Free antigen and antibody (IgG or IgM) combine in the presence of complement and precipitate as immune complexes, causing tissue destruction

38
Q

Examples of type 3 hypersensitivity

A
  • Endogenous antigens (serum sickness, drug-induced haemolytic anaemia)
  • Microbial antigens (post-streptococcal GN)
  • Autologous antigens (RA, SLE, polyarteritis nodosa)
39
Q

Define type 4 hypersensitivity

A

Cell-mediated hypersensitivity involving specifically primed T-lymphocytes

40
Q

Examples of type 4 hypersensitivity

A
  • Chronic organ rejection
  • Contact dermatitis
  • Microbial agents (TB, viruses, funghi)
41
Q

Mnemonic for hypersensitivity reactions

A

A - antibody (IgE) mediated
C - cytotoxic
I - immune-complex
D - delayed

42
Q

Define autoimmunity

A

Immune response against a self-antigen

43
Q

Genetic susceptibility to autoimmune diseases

A

Alleles of MHC class 2 (HLA-D region)

44
Q

Role of HLA Class 1 molecules

A

HLA-A and HLA-B induce formation of complement-fixing cytotoxic antibodies and act as cell surface recognition markers for cytotoxic T-cells

45
Q

Where are HLA class 1 antigens present in Kidney grafts

A
  • Vascular endothelium
  • Interstitial cells
  • Mesangial cells
  • Tubular epithelium
46
Q

Role of HLA Class 2 molecules

A

Activates CD4+ T-helper cells, which begins the process of clonal expansion

47
Q

Where are HLA Class 2 antigens expressed

A

Surface of:

  • B-cells
  • Macrophages
  • Activated T-cells
  • APCs
48
Q

Define the two phases of allograft rejection

A
  1. Afferent (sensitisation) phase

2. Efferent (effector) phase

49
Q

Describe the afferent phase of allograft rejection

A
  • Donor MHC molecules on graft are recognised by recipient CD4+ T-cells
  • Recipient helper T-cells recognise donor MHC molecules that have been processed by APCs
  • T-cell proliferation occurs
50
Q

Describe the efferent phase of allograft rejection

A
  • CD4+ T-cells (helper T-cells) enter the graft and recruit cells responsible for the tissue damage of rejection
  • Cells recruited include B-lymphocytes, macrophages, natural killer cells, CD8+ T-cells (cytotoxic)
  • Activated cytotoxic cells damage the graft cells by proteolytic action (Granzyme B and Perforin)
51
Q

Describe hyperacute rejection

A
  • Occurs within minutes-hours - ABO incompatibility or preformed cytotoxic antibodies from previous transplant/transfusion
  • Complement is activated
  • IgG and C3 bind to endothelial cells
  • Graft loss occurs
52
Q

What antibody mediates hyperacute rejection

A

IgG

53
Q

Describe the histological signs of acute rejection

A

Infiltration of tubules and interstitium by cytotoxic T-cells, which destroy the graft

54
Q

Timeframe of acute rejection

A

Between 1 week and 3 months (commonest at 7-10 days)

55
Q

Describe the histological signs of chronic renal graft rejection

A

Thickening of the GBM, hyalinisation of glomeruli, intimal hyperplasia, tubular atrophy, and interstitial fibrosis

Pathology (7 decks)

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