Immunoparasitology Flashcards
Ectoparasite vs endoparasite
Ectoparasite: lives on surface of host (lice, ticks, mites)
Endoparasite: lives inside host (Toxoplasma gondii)
Obligate vs Facultative parasite
Obligate: completely dependent on host during part/ all of its life cycle (Plasmodium sp.)
Facultative: exhibits both parasitic + free-living stages (doesn’t completely depend on host for survival ie. Naglaria fowleri)
Accidental vs Erratic parasites
Accidental: infects an unnatural host and survives (Hymenolepis diminuta)
Erratic: migrates improperly and ends up in host tissues where it is not usually found (Trichinella spiralis)
Direct impacts on host
- mechanical injury (migration, growth = blockage)
- toxic substances (waste + immunological distractions)
- nutrient deprivation (competes for iron, energy, water)
- anemia (consumption/ destruction of RBCs
Indirect impacts on host
- inflammation (parasite presence or released molecules)
- encapsulation (granuloma formation)
- reduced cognitive capability
3 stages of immune response to parasites
- Initial exposure
- complement targets parasite for encapsulation + phagocytosis
- previous exposure may have resulted in circulating antibodies
- parasites can encounter immune cells during migration - Establishment of Infection
- tissues: cellular defence + inflammation
- blood: cellular defences, antibody, circulating defence molecules, complement
- gastrointestinal: IgA, antimicrobial peptides, physical environment - Chronic
- long-term infections usually evades immune system
Neutrophil response to parasites
- Oxidative burst
- Degranulation:
— Primary: Myeloperoxidase, bacteriacidal, permeability-increasing protein, defensins, elastase
— Secondary: alkaline phosphatase, lysosome, collagenases
— Tertiary
Eosinophil response to parasites
- associated with worm infections too large for phagocytosis
- degranulate when surface Fc receptors recognize IgE (enhanced by cytokines ie. TNF-a)
- often acts with Mast cells bc of IgE detection
Phagocytosis response to parasites
- tissue macrophages, monocytes, and granulocytes can be engaged before cytokine production or antibody response is generated
- remove protozoans and encapsulate small multicellular parasites
= inflammation
= production of cytokines
= facilitates breakdown of pathogen so it can be presented on MHC II
Inflammation response to parasites
- production of reactive oxygen and nitrogen species
- cytokines that initiate a signalling cascade
= activation of immune cells
= production of more anti-pathogen effectors
IgE
- shortest half-life (2.5 days) = least common serum antibody
- high affinity with mast cell, basophil, and eosinophil Fc receptors
- DOES NOT BIND COMPLEMENT
= immunity to helminth (Schistosoma mansoni, Trichinella spiralis) + protozoan parasites (Plasmodium sp.)
= associated with allergy and hypersensitivity = anaphylaxis
IgE interaction with Mast Cells
Mast cell: critical for helminth defence
- tissue + mucosal
IgE-activated:
- degranulation = serine proteases, histamines, serotonin, anticoagulant (heparin), platelet activating factor, cytokine, eosinophil chemotactic factor
= extensive swelling, vasodilation, inflammation and pain/ itching
= allergic response = anaphylaxis if primed by high IgE
Antibody-Dependent Cell-mediated Cytotoxicity
- innate effector cells (NK, eosinophil, neutrophil) recognizes antigen-bound antibodies on parasite surface
- mediated through recognition of Fc portion of an antibody by a cell-surface Fc receptor with IgG or IgE = cytokine release (IFN-y, perforin, granzymes) = apoptosis
- important for defence against larger helminth parasites (too large for phagocytosis)
IL-4 and IL-13
- released by Th2 cells
- causes B cells to produce IgE
- IgE interacts with mast cell = degranulation AND worm killing
