Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Immune system
| Term | Definition |
|---|---|
| Protective immunity in blood/lymph/interstitial space | Complement, phagocytosis, Ab (innate/adaptive) against viruses, bacteria, protozoa, fungi, worms |
| Protective immunity on epithelial surfaces | Antimicrobial peptides, IgA against Streptococcus pneumoniae, Neisseria gonorrhoea, Vibrio cholerae, Helicobacter pylori, worms |
| Protective immunity in cytoplasm | NK cells (innate), CTL (adaptive) against viruses, Chlamydia, Ricketts, protozoa |
| Protective immunity in vesicles | T/NK cell dependent macrophage activation (cytotoxic) against Mycobacterium, Yersinia pestis (plague) |
| Innate immunity characteristics | In place prior to infection -> immediate reaction, recognise pathogen nature -> pass info to adaptive, no memory, hard-coded, non-specific |
| Adaptive immunity characteristics | Slow development (days), memory, acquired, highly specific via somatic recombination |
| Innate barriers | Skin, mucosal epithelia, anti-microbial chemicals |
| Adaptive barriers | Epithelial lymphocytes, Ab secretion |
| Innate cells | Phagocytes (neutrophils/macrophages), eosinophils, mast cells, NK cells |
| Adaptive cells | T/B lymphocytes |
| Innate soluble components | Complement, cytokines, acute phase proteins, inflammatory mediators |
| Adaptive soluble components | Ab (immunoglobulins) |
| Innate immunity timeframe/process | 0-4 hrs, recognition via preformed non-specific effectors |
| Early induced innate response timeframe/process | 4-6 hrs, effector cell recruitment -> pathogen recognition -> effector cell/inflammation activation |
| Adaptive response timeframe/process | >96 hrs -> Ag transport to lymphoid organs -> B/T cell naive recognition -> effector B/T cell expansion/activation |
| Tissue injury sterotypical response | Eliminate initial cause of cell injury -> remove necrotic tissue from insult/subsequent immune response -> initiate damaged tissue repair |
| Acute inflammatory exudate recruitment rationale | Leucocytes/soluble factors may eliminate pathogen |
| Inflammation characteristics | Calor (heat - increased blood flow to acute inflammatory site), dolor (pain - nerve ending stimulation), rubor (redness -> increased circulation/vasodilation), tumour (swelling -> increased tissue fluid), clinician adds loss of function |
| Acute phase systemic responses to serious infections | Fever, neutrophilia (increase in circulating neutrophils), increase in plasma acute phase proteins |
| Stratified squamous epithelial skin characteristics | Tight junctions, keratin, dry hostile environments (limit bacterial growth), regular desquamation (resist invasion), epithelial cells produce fatty acids, lamellar bodies, beta-defensins (inhibit microbial growth/proliferation) |
| Mucosal glandular epithelia of GI/respiratory tract characteristics | Cilia, goblet cells (mucin secretions trap microbes), tight junctions, unidirectional fluid flow (impede microbial adhesion/facilitate pathogen removal), low pH, enzymes, defensins |
| Secretion examples | Glandular surface mucus, stomach acid (low pH), antimicrobial peptides (defensins/cathelicidins - damage microbe membranes), enzymatic lysosymes in tears/saliva, pepsin in stomach |
| Haematopoeitic stem cells differentiate into? | Common lymphoid/myeloid precursors |
| Common lymphoid precursors differentiate into? | B cell -> plasma cell, NK/T-cell precursor -> NK cell and T cell -> effector cell |
| Common myeloid precursors differentiate into? | Granulocyte/macrophage progenitor and megakaryocyte/erythroid progenitor |
| Granulocytes differentiate into? | Macrophage/dendritic cell precursor, neutrophil, eosinophil, basophil, mast cell |
| Macrophage/dendritic cell precursors differentiate into? | Monocyte -> macrophage, dendritic cells |
| Megakaryocyte/erythroid progenitors differentiate into? | Megakaryocyte -> platelets, erythroblast -> RBCs |
| Neutrophil physical characteristics | 60% plasma, multi-lobed nucleus, poorly stained granules, short-lived |
| Neutrophil immune characteristics | Mobilise to infection sites via chemotaxins (C5a/fMLF), phagocytosis, degranulate -> release antibacterial proteins, extrude DNA -> NETs to limit spread, form pus -> nucleic acid leak |
| Eosinophil physical characteristics | 3% plasma, bi-lobed nucleus, pink stained granules |
| Eosinophil immune characteristics | Non phagocytic, defence against helminth worms (Th2) |
| Basophil physical characteristics | 1% plasma, bi-lobed nucleus, blue stained granules |
| Basophil immune characteristics | Non phagocytic, IL-4 source -> Th2 |
| Mast cell physical characterstics | Sentinel cells beneath epithelial surfaces in connective/mucosal tissue, blue stained oval nucleus, purple stained cytoplasmic granules |
| Mast cell immune characteristics | Preformed histamine in secretory granules -> degranulate post-activation -> histamine works on vascular endothelium -> dilate blood vessel/increase permeability -> rapid inflammation, flare-and-wheal |
| Mast cell activation | Allergens -> IgE cross-linking, PAMPs/DAMPs, complement C3/5a, substance P (neurogenic inflammation) |
| Monocyte physical characteristics | 6% plasma, large cells, bean shaped nucleus, sentinel cells beneath epithelial surfaces |
| Monocyte immune characteristics | Mature into macrophages in tissues, phagocytosis |
| M1 macrophage characteristics | Secrete cytokines/pro-inflammatory mediators -> acute inflammatory response |
| M2 macrophage characteristics | Tissue repair, parasite killing/expulsion |
| Monocyte activation | Differential activation -> different responses -> plasticity -> change physiology in response to environmental cues |
| Dendritic cell immune activation and function | Bridge innate/adaptive system, Langerhans cells phagocytose pathogens at peripheral infection site -> take on DC morphology -> carry encounter record to lymph node DCs -> activate specific B/T cells |
| NK cell physical characteristics | Large circular dark-staining nucleus, light-purple staining cytoplasmic granules |
| NK cell activation | Partially activated in blood circulation -> proliferate in affected tissue -> viral infections |
| How do NK cells recognise infection/cell damage? | Missing-self or induced-self models |
| What is the missing-self model? | Loss of molecules that normal cells express -> viruses inhibit MHC class I expression to evade immune system -> NK cells recognise missing self lack of MHC |
| What is the induced-self model | Cells express stressed-induced self-molecules -> ligands for NK activating receptors -> activation > healthy inhibitory signals |
| How are NK cells activated? | Type I IFN cytokines -> increase activating ligand expression, macrophage cytokines (CXCL8, IL-12/15) -> NK proliferation/maturation (fully activated) |
| How does NK degranulation work? | Released perforin forms PM pores -> apoptosis-inducing granzymes released intracellularly |
| What are NK effector functions? | Degranulation, Ab dependent cell cytoxicity, cytokine release |
| How does ADCC work? | Viral proteins bound by Ab -> NK cells have FcR to activate NK cells |
| How does NK activate macrophages? | Activated NK cells release IFN-γ -> activate macrophages -> upregulate macrophage/NK cell killing capacity -> initiate adaptive immune response |
| Innate lymphoid cell characteristics | Don't have B/T cell Ag receptors, don't directly control infection like NK cells, amplify signals produced in innate recognition |
| ILC1 characteristics | Stimulated by IL-12/15/1B -> release IFN-γ cytokine -> activate M1 macrophage/type 1 immune response against viruses/intracellular pathogens |
| ILC2 characteristics | Stimulated by IL-25/33 -> release IL-4/5/13 cytokine -> activate M2 macrophage/type 2 immune response -> mucus production/vasodilation/ECM repair against parasite/helminth |
| ILC3 characteristics | Stimulated by IL-1B/23 -> release IL-17/22 cytokine -> activate type 3 immune response -> phagocytosis/antimcrobial peptides against extracellular bacteria/fungi |
| Cytokine features | Redundancy -> several cytokines w/ same function, pleiotropism -> single cytokine have different functions, antagonism -> cytokines block another, synergism -> cytokines work together for greater sum effect |
| How many Janus kinases? | 4 - intracellular non-receptor Tyr K -> 2 near identical phosphate transferring domains (activating/inhibitory) |
| How many STATs? | 7 - signal transducer and activator of transcription |
| Jak-STAT pathway | Cytokine binds to multi-subunit cytokine receptors -> pull subunits together -> Jak protein binds receptor -> STAT protein binds to JAK -> dimerises -> translocates to nucleus as TF |
| Histamine features | Generated from histidine, stored in mast cell granules, basophils, eosinophils, acts on vascular endothelium -> capillary vasodilation |
| How are acute phase proteins released? | Macrophage activation -> IL-6 cytokine production -> triggers hepatocytes to release acute phase proteins -> CRP/fibrinogen |
| CRP function | Trigger opsonin/complement activation -> monitored in blood samples to determine infection presence |
| Fibrinogen features | Fibrin clot formation -> haemostasis/infection control -> thrombin converts soluble fibrinogen into insoluble fibrin strands entrapping bacteria -> limit growth/dissemination -> support host cell recruitment/activation |
| Defensin features | Antimicrobial peptides -> disrupt bacteria/fungi/enveloped virus membranes -> neutralise toxins (promote unfolding) -> aid host protease attack |
| Pentraxin features | Serum amyloid P component -> PTX3 -> binds to pathogens/phagocytic receptor CD89 (IgA) -> similar role as Ab -> determine infection presence |
| Arachidonic acid metabolite features | Derived from cell membrane phospholipids, released in tissue damage -> potent inflammatory mediators -> PG/leukotrienes |
| PG features | AA -> immediate cyclo-oxygenase pathway -> PG -> vascular permeability/dilation, neutrophil chemotaxis |
| Leukotriene features | AA -> delayed lipo-oxygenase pathway -> leukotrienes -> histamine backup (slow but 100x potent) |
| Leukotriene disadvantages | Initial asthma attack -> breathing problems from histamine -> leukotriene/PG production kicks in -> inflammation/bronchoconstriction/mucus production -> debilitating restriction in airway capacity -> lower breathing V -> anaphylactic shock |
Created by:
vykleung
Popular Pathology sets