Lecture 26 - Immunity and Infection Flashcards

1
Q

Factors of immunity and infection - microbial?

A

type, virulence, amount, route of entry

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2
Q

Factors of immunity and infection - host?

A

integrity of innate barriers, adaptive immune competence, HLA, Ig and TCR genes, previous exposure, other infections

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3
Q

Pathogens and antigens - viruses?

A

capsid antigens or HLA I presented metabolic or internal structured components

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4
Q

Pathogens and antigens - bacteria and fungi?

A

extracellular (aureus) or intracellular (m. tuberculosis), structural components and metabolic components and toxins

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5
Q

Cytotoxic T cells vs antibodies?

A

rather than antigens outside cells of body (toxins, bacteria, viruses), is effective against intracellular protein antigens (viral cytoplasmic peptides, tumour cells, transplanted organs)

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6
Q

Complement cascade?

A

DRAW IT MOTHER FUCKER

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7
Q

Immunity to bacteria - antibodies and complement?

A

prevent adherence or reduce mobility, enhance bacterial destruction (complement), enhance phagocytosis (opsonisation)

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8
Q

Bacterial tactics to avoid antibodies?q

A

opsonisation resistant capsules e.g. Haemophilus influenzae, intracellular growth e.g. M tuberculosis

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9
Q

Mucosal immunity?

A

IgA in mucosa first blockade, then IgE presenting mast cells detect antigen and release vasoactive and chemotactic factors, causing blood vessels to release IgG, complement, neutrophils and eosinophils

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10
Q

Receptors of K/NK cells?

A

Fc(gamma) receptor for ADCC, killer-activating and killer-inhibitory receptor for natural killing activity

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11
Q

NK cell physiology?

A

binding of killer-inhibitory receptro to HLA I gives no action, lack of binding leads to cell killing, enhanced by IL-2 and IFN-(gamma), important in early viral infection and cancer

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12
Q

Acute viral infection?

A

virus amount on the rise, interferon from infected cells rise accordingly, Nk activity follows suit, delay then cytotoxic T cells have been formed and rise, antibodies rise last and are to prevent re-infection rather than fight illness

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13
Q

Pro-inflammatory cytokines?

A

early, induce acute phase proteins, fever and behavioural changes, tissue repair (bone reabsorption, fibroblast proliferation, collagenase synthesis, leukocyte adhesion), T and B cell activation

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14
Q

Chemokines?

A

aid chemotaxis, direct effector cell traffic

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15
Q

Interferons?

A

induce transient antiviral state, activate NK cel activity, upregulate MHC expression (therefore improving cytotoxic T cell killing)

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