Response to Infectious Agents Flashcards
Sterilizing Immunity
immunity conferred by vaccination that prevents infection or colonization of pathogen on animal
highest degree of protection achievable by vaccine
Protective Immunity
immunity that protects an animal against infection &/or infectious disease.
not all immune responses are protective
Humoral Immunity
- mediated by Abs
- effective vs. extracellular phase of pathogens
- better at inhibiting infection & reducing spread
Cell-Mediated Immunity (CMI)
- mediated by T-cells
- effective vs. intracellular phase (also extracellular when inside)
- better at clearing infection.
Pathogens are exposed to ___ on adherence to epithelium the 1st time.
antimicrobial peptides, phagocytes, microbiota
Pathogens are exposed to ___ upon penetration of epithelium (local infection) the 1st time.
Antimicrobial peptides, phagocytes, complement
Pathogens are exposed to ___ in a local infection the 1st time.
inflammation
Pathogens are exposed to ___ during adaptive immunity the 1st time.
Humoral & Cell-mediated immunity
Pathogens are exposed to ___ on adherence to epithelium on subsequent exposures.
sIgA
antimicrobial peptides
phagocytes
microbiota
Pathogens are exposed to ___ upon penetration of epithelium on subsequent exposures.
IgG
Antimicrobial peptides
phagocytes
complement
Pathogens are exposed to ___ in local infection on subsequent exposures.
Inflammation
IgM, IgG
Th1, Th2, Th17, Tc
Sterilizing vaccines are really good at…
secreting lots of IgG for neutralization systemically.
Extracellular Protective Immunity
interstitial spaces, blood, lymph
complement, phagocytosis, antibodies
Extracellular Protective Immunity
epithelial surfaces
antimicrobial peptides, Abs (esp. IgA)
Intracellular Protective Immunity
cytoplasmic
NK cells, Cytotoxic T-cells
Intracellular Protective Immunity
vesicular
T cell & NK cell dependent macrophage activation
Mucosal Immunity involves
respiratory & intestinal systems
Innate Respiratory Mucosal Immunity cells
-ciliated columnar epithelium with goblet cells
Innate Respiratory Mucosal Immunity chemicals
lysozymes, defensins, surfactants
Innate Respiratory Mucosal Immunity specializations
mucociliary escalator
Innate Respiratory Mucosal Immunity phagocytes presented in:
lamina propria & alveolar macrophages
Innate Intestinal Mucosal Immunity cells
columnar epithelium with goblet cells
Innate Intestinal Mucosal Immunity chemicals
lysozymes, defensins, gastric acidity, bile enzymes
Innate Intestinal Mucosal Immunity specializations
peristalsis
Innate Intestinal Mucosal Immunity phagocytes present in:
lamina propria
Adaptive Mucosal Immunity - humoral
secretory IgA
Adaptive Mucosal Immunity - cell-mediated
intraepithelial lymphocytes & lamina propria lymphocytes
Extracellular pathogen Adaptive immunity type
humoral more important than cell-mediated
Innate Immunity against extracellular pathogens
epithelial cleansing mechanisms
mucociliary elevator, intestinal peristalsis, flow of uring, tears & eyelashes, saliva, cough reflex
Innate Immunity against extracellular pathogens
Antimicrobial Molecules
defensins, lysozymes: kill many pathogens
epidermal fatty acids: inhibit growth
Gastic acidity: inhibits growth
Innate Immunity against extracellular pathogens
most important innate defense against them =
professional phagocytes
Complement against Extracellular Pathogens
contributes some but its major role is helping with inflammation & opsonization
Adaptive Immunity against Extracellular Pathogens uses:
secretory IgA, IgG, Th17 cells
Secretory IgA against Extracellular pathogens
exclusion of pathogens at mucosal surfaces
IgG against extracellular pathogens
opsonizing Abs are important for phagocytosis & maybe ADCC
TH17 cells & extracellular pathogens
they recruit & activate neutrophils to combat extracellular pathogens
Helminth’s important Ags
the ones secreted & captured by DCs in intestines
larval form of helminths require
humoral immunity b/c they migrate through interstitial tissues
Innate mechanisms for helminths
mast cells, histamine & other MC mediators, eosinophils, mucus/peristalsis
Mast cell against helminths
release histamine when IgE binds helminth Ags
Histamine & other MC mediators against helminths
- induce local inflammation
- increase mucus secretion & peristalsis to expel adults
Eosinophils against Helminths
- recruited by chemokines from mast cells & Th2.
- mediate ADCC (IgE, IgG)
- granules contain antimicrobial substances that’re effective against helminths
Mucus & Peristalsis against Helminths
create less hospitable environment. may induce detachment & expulsion of some
Adaptive Mechanisms used with Helminths
IgE, IgG, Th2
IgE + helminths
bind to Fce receptors on mast cells, activate mast cells when Ags bind.
mediate ADCC for eosinophils
IgG + Helminths
mediates ADCC for eosinophils for migrating larva
TH2 cells + helminths
promote IgE secretion by B cells
activate eosinophils to attack egg/larva
most important defense agains intracellular pathogens
Cell-mediated immunity
innate epithelial cleansing mechanisms + intracellular pathogens
mucociliary elevator, intestinal peristalsis, flow of urine, tears & eyelashes, saliva, cough reflex
innate antimicrobial molecules + intracellular pathogens
defensins, lysozymes: kill many pathogens
epidermal fatty acids: inhibit growth
gastric acidity: inhibit growth
innate macrophages + intracellular pathogens
pathogens can resist most killing mechanisms.
macrophages must be activated by IFN-gamma & make NO to kill them
innate NK cells + intracellular pathogens
early source of INF-gamma. may kill infected cells
Adaptive cells involved against intracellular pathogens
Th1, Tc
Th1 cells + intracellular pathogens
release IFN-gamma & recruit fresh macrophages that are better prepared to kill
Tc cells + intracellular pathogens
- kill infected cells & release pathogen.
- pathogen binds to Abs & newly recruited, IFN-gamma primed macrophages ingest it.
important immunity against viruses
humoral and cell-mediated
Innate mechanisms against viruses
Interferons alpha, beta, omega
NK cells
Adaptive mechanisms against viruses
secretory IgA, IgG, Tc cells
Interferons alpha, beta, omega + viruses
- released from infected wrt different stimuli.
- IFN binds to receptors on adjacent cells
- adjacent cells make new proteins that viral nucleic acids activate
- antiviral IFN effects: degradation of viral mRNA & inhibit translation
- increase MHC expression; activate DC, macrophages, NK cells
NK cells + viruses
primary effect: kill infected cells
- viruses make cells make stress proteins that activate NK cells & reduce MHC I expression which inhibits NK activation
- NK cells release IFN-gamma which activates macrophages
secretory IgA + viruses
sIgA neutralizes viruses at surface where they enter & inhibits establishment or spread of infection
IgG + viruses
neutralizing IgG important SYSTEMICALLY
many vaccines done this way (ex: parvoviruses)
Tc Cells + viruses
Tc kill infected cells & limit viral replication
main contribution = after establishment of viral infection b/c only act after cells are infected
viral replication process
- Attachment 2. Penetration 3. Uncoating 4. Non-Structural Proteins made 5. Genome Replication 6. Structural Proteins made 7. Assembly 8. Release
