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Flashcards in 1. Hypersensitivity Deck (12)
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1

define 'hypersensitivity'

The ANTIGEN-SPECIFIC immune responses that are either inappropriate or excessive and result in harm to the host.

2

describe the 2 common phases of all hypersensitivity reactions

1. SENSITISATION phase
- 1st encounter with Ag
- causes activation of APCs and memory effector cells

2. EFFECTOR phase
- pathologic reaction upon re-exposure to same Ag and activation of memory effector cells of adaptive immunity
- causes clinical manifestation

3

describe the antigen and antibodies involved in the 4 types of hypersensitivity

Type I - immediate (Allergy)
- response to environmental non-infectious Ag
- involves IgE

Type II - anti-Body mediated
- response to cell-bound Ag
- involves IgG or IgM
- develops in 5-12 hrs

Type III - immune-Complex mediated
- response to soluble Ag
- involves IgG or IgM
- develops in 3-8 hrs

Type IV - cell-mediated (Delayed)
- response to environmental infectious Ag and self Ag
- involves cellular response
- develops in 24-72 hrs

4

what are the 2 possible mechanisms of disease involved in T2HS

1. tissue/cell damage
- complement activation: cell lysis (MAC), neutrophil recruitment/activation (C3a/C5a), opsonisation
- Ab-dependent cell cytotoxicity (ADCC, IgG)

2. Physiological change
- receptor stimulation (e.g. Ag bind and activate TSH R - Graves' disease)
- receptor blockade (e.g. Ag bind and block ACh R - Myasthenia gravis)

5

Suggest 4 possible therapeutic approaches to T2HS-mediated tissue/cell damage

1. immune suppression (prevent complement activation)
2. plasmapheresis (remove circulating antibodies and inflammatory mediators) - allows short-term relief and healing of damaged tissue
3. splenectomy (prevent opsonisation/phagocytosis)
4. intravenous immunoglobulin (IVIG, blockage of macrophage Fc Rs)

6

what is the pathogenesis underpinning T3HS

tissue damage caused by:
a) immune complex deposition in tissue...
b) complement activation...
c) neutrophil chemotaxis...
d) neutrophil adherence and degranulation

7

name 3 factors affecting IC pathogenesis in T3HS

1. complex size: small and large size ICs cleared whilst intermediate size ICs persist

2. host response
- low affinity antibody (form intermediate ICs)
- complement deficiency (large complement activation in T3HS causes tissue damage)

3. local tissue factors
- haemodynamic factors
- physiochemical factors

Result in persistence of IC deposition in joints, kidneys, small vessels and skin - multisystem disease

8

name 3 examples of T3HS and their causative Ag

1. rheumatoid arthritis (auto-immune):
- Ag = Fc portion of altered IgG
- Ab = rheumatoid factor (IgM)

2. Glomerulonephritis (infectious), e.g. bacterial endocarditis, HepB infection

3. Systemic lupus erythematosus
- Ag = ds-DNA

9

which 2 cell types are mainly involved in T4HS

lymphocytes and macrophages

10

describe 3 subtypes of T4HS and name examples of diseases

1. contact hypersensitivity
- 48-72 hrs
- epidermal reaction (eczematous rash)
- e.g. nickel, poison ivy, organic chemicals

2. tuberculin hypersensitivity
- 48-72 hrs
- dermal reaction (induration and swelling)
- e.g. Mtb

3. granulomatous hypersensitivity (most severe)
- 21-48 days
- persistence of Ag (tissue damage) causes granuloma formation to wall off infected cells
- e.g. tuberculosis, leprosy, schistosomiasis, sarcoidosis

11

name 3 diseases caused by T4HS to endogenous Ag

1. pancreatic islet cells - insulin-dependent diabetes mellitus

2. thyroid gland - Hashimoto's thyroiditis (involvement of CD8+ T cells and antibodies)

3. IgG - RA

12

suggest 2 main classes of drugs used to treat T3 and T4HS

1. anti-inflammatory drugs
- NSAIDs
- corticosteroids (oral prednisolone)
- 2nd drugs as steroid-sparing agents (<10mg oral steroid), e.g. azathioprine, mycophenolate mofetil, cyclophosphamide

2. monoclonal antibodies
- B and T cells
- cytokine network
- APCs