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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
What must antigens be presented alongside to be recognised by T-cells
MHC class 2 antigen
26
What activates the 'classical' complement pathway
Antigen-antibody (immunoglobulin) complexes
27
What activates the 'alternative' complement pathway
Bacterial cell surfaces
28
What is the outcome of both complement pathways
Production of membrane attack complexes
29
List the functions of complement
- 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
How can immune deficiency be classified
- Specific deficiencies | - Non-specific deficiencies
31
How are specific immune deficiencies divided
1. Primary = due to an intrinsic defect in the immune system (usually genetic) 2. Secondary = due to an underlying condition
32
Define type 1 hypersensitivity
Immediate hypersensitivity due to overproduction of IgE on mast cells of basophils
33
Examples of type 1 hypersensitivity
- Asthma - Hayfever - Allergic rhinitis
34
Define type 2 hypersensitivity
Cytotoxic - antibody to cell-bound antigen
35
Examples of type 2 hypersensitivity
- Transfusion reactions - Rhesus incompatibility - Autoimmune haemolytic disease - ITP - Myasthenia gravis - Goodpasture's syndrome
36
Define type 3 hypersensitivity
Deposition of immune complexes in the tissues
37
Pathophysiology of type 3 hypersensitivity
Free antigen and antibody (IgG or IgM) combine in the presence of complement and precipitate as immune complexes, causing tissue destruction
38
Examples of type 3 hypersensitivity
- Endogenous antigens (serum sickness, drug-induced haemolytic anaemia) - Microbial antigens (post-streptococcal GN) - Autologous antigens (RA, SLE, polyarteritis nodosa)
39
Define type 4 hypersensitivity
Cell-mediated hypersensitivity involving specifically primed T-lymphocytes
40
Examples of type 4 hypersensitivity
- Chronic organ rejection - Contact dermatitis - Microbial agents (TB, viruses, funghi)
41
Mnemonic for hypersensitivity reactions
A - antibody (IgE) mediated C - cytotoxic I - immune-complex D - delayed
42
Define autoimmunity
Immune response against a self-antigen
43
Genetic susceptibility to autoimmune diseases
Alleles of MHC class 2 (HLA-D region)
44
Role of HLA Class 1 molecules
HLA-A and HLA-B induce formation of complement-fixing cytotoxic antibodies and act as cell surface recognition markers for cytotoxic T-cells
45
Where are HLA class 1 antigens present in Kidney grafts
- Vascular endothelium - Interstitial cells - Mesangial cells - Tubular epithelium
46
Role of HLA Class 2 molecules
Activates CD4+ T-helper cells, which begins the process of clonal expansion
47
Where are HLA Class 2 antigens expressed
Surface of: - B-cells - Macrophages - Activated T-cells - APCs
48
Define the two phases of allograft rejection
1. Afferent (sensitisation) phase | 2. Efferent (effector) phase
49
Describe the afferent phase of allograft rejection
- 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
Describe the efferent phase of allograft rejection
- 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
Describe hyperacute rejection
- 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
What antibody mediates hyperacute rejection
IgG
53
Describe the histological signs of acute rejection
Infiltration of tubules and interstitium by cytotoxic T-cells, which destroy the graft
54
Timeframe of acute rejection
Between 1 week and 3 months (commonest at 7-10 days)
55
Describe the histological signs of chronic renal graft rejection
Thickening of the GBM, hyalinisation of glomeruli, intimal hyperplasia, tubular atrophy, and interstitial fibrosis

Pathology (7 decks)

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