Infection and Immunity

Question 1

Things that alter how an infection is responded to? microbial and host factors

Answer 1

Microbial: type or organism, dose, virulence, route of entry

Host: innate system, adaptive system, HLA, Ig and TCR genes, previous exposure and other infections

Question 2

Pathogens and antigens: Virus, bacteria (and fungi), parasites

Answer 2

• Virus: lytic or integrated cycle, capsid antigens, internal structural and metabolic components on HLA 1
• Bacteria (and fungi): extracellular( S.aureus) or intracellular TB, structural components, metabolic products, toxins
• Parasites: large (multicellular), life cycle changes, radical changes in antigenicity

Question 3

Immune factors involved with infection

Answer 3

Direct neutralisation
Opsonisation
Complement
T cell mediated cytotoxicity
NK cells
Inflammatory and immunoregulatory cytokines
Antiviral interferons

Question 4

Antibodies are effective against

Answer 4

Antigens outside cells: Viruses (A,G,M), toxins(G,M), extracellular bacteria(A,M,G), parasites (E, A)

Question 5

Cytotoxic T cells effective against

Answer 5

Intracellular protein antigens: Virus infections, tumour cells, organ transplants

Question 6

Bacterial pathogen initial reaction

Answer 6

PAMPs such as LPS and peptidoglycans recognised leading to:
Vascular permeability changes, phagocyte recruitment, APP induction, local temp change
Leads to phagocytosis and complement activation

Question 7

Immunity to bacteria is conducted by what?

Answer 7

Antibodies and complement: preventing adherence or reducing mobility, destroying by complement or opsonisation

Some avoid antibody effects: capsule resistant opsonisation, and some do intracellular growth

Question 8

Mucosal immunity

_____ cells in gut for example can produce surface___ to block _____ and opsonise.
In ___ itself, some ___ cells with ___ releasing ____ and chemotactic factors, causing ___, _____, _____ and eosinophils to move to pathogen zone

Answer 8

Epithelial cells in gut for example can produce IgA to block adherence and opsonise.
In tissue itself, some mast cells with IgE releasing vasoactive and chemotactic factors, causing IgG, complement, neutrophils and eosinophils to move to pathogen zone

Question 9

How do NK cells kill?

• Antibody dependent cellular cytotoxicity through the ____ receptor (____)
• Natural killing activity: Killer ____ and killer ____ receptors. Killer _____ receptor will bind to a _____ receptor on a cell, and killer ____ receptor binds to ____ molecule. If it does not bind a ____ in an abnormal cell (tumour, infected) will ____

Answer 9

• Antibody dependent cellular cytotoxicity through the Fcy(gamma) receptor (CD16)
• Natural killing activity: Killer activating and killer inhibitory receptors. Killer activating receptor will bind to a ubiquitous receptor on a cell, and killer inhibitory receptor binds to HLA 1 molecule. If it does not bind a HLA 1 in an abnormal cell (tumour, infected) will kill

Question 10

NK cell features

Answer 10

Exhibit ADCC
Killer inhibitory receptor binds HLA 1
Activity enhanced by IL-2 and IFN-y
Early in viral infections, and cancer

Question 11

Acute viral infection response

Answer 11

Pg180

• Interferon peak first
• This up regulates NK cell activity
• Cytotoxic T cells come a little later due to activation
• Antibodies work last and act mainly by preventing re infection and infection spread