Lecture 26 - Immunity and Infection Flashcards
Factors of immunity and infection - microbial?
type, virulence, amount, route of entry
Factors of immunity and infection - host?
integrity of innate barriers, adaptive immune competence, HLA, Ig and TCR genes, previous exposure, other infections
Pathogens and antigens - viruses?
capsid antigens or HLA I presented metabolic or internal structured components
Pathogens and antigens - bacteria and fungi?
extracellular (aureus) or intracellular (m. tuberculosis), structural components and metabolic components and toxins
Cytotoxic T cells vs antibodies?
rather than antigens outside cells of body (toxins, bacteria, viruses), is effective against intracellular protein antigens (viral cytoplasmic peptides, tumour cells, transplanted organs)
Complement cascade?
DRAW IT MOTHER FUCKER
Immunity to bacteria - antibodies and complement?
prevent adherence or reduce mobility, enhance bacterial destruction (complement), enhance phagocytosis (opsonisation)
Bacterial tactics to avoid antibodies?q
opsonisation resistant capsules e.g. Haemophilus influenzae, intracellular growth e.g. M tuberculosis
Mucosal immunity?
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
Receptors of K/NK cells?
Fc(gamma) receptor for ADCC, killer-activating and killer-inhibitory receptor for natural killing activity
NK cell physiology?
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
Acute viral infection?
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
Pro-inflammatory cytokines?
early, induce acute phase proteins, fever and behavioural changes, tissue repair (bone reabsorption, fibroblast proliferation, collagenase synthesis, leukocyte adhesion), T and B cell activation
Chemokines?
aid chemotaxis, direct effector cell traffic
Interferons?
induce transient antiviral state, activate NK cel activity, upregulate MHC expression (therefore improving cytotoxic T cell killing)