IMM2022 Lecture Notes - Lecture 9: Leishmaniasis, Eosinophil, Degranulation
30 May 2018
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PARASITES
Parasite: organism that lives/feeds off another organism (host) without providing any benefit to the
host
Protists: single celled animal-like eukaryotic organisms
The immune system fights extracellular pathogens by antibodies that opsonise and label pathogens
with IgG that are recognised by Fc receptors on phagocytes (activates phagocytosis).
• Antibodies also activate complement that can lyse extracellular pathogens and also opsonisation
• Intracellular pathogens:
o Th1 cells activate macrophages via cytokine IFNg and surface molecule CD40L
macrophages -> activate respiratory burst -> secrete pro-inflammatory cytokines (TNF, IL-1,
IL-12) -> upregulating MHC and costimulatory molecules
o Cytotoxic: recognise peptide on MHC I and kill effector cells by release of cytotoxic granules
that contain perforin and granzymes
o Antibodies play no role in intracellular pathogens but can neutralise
Trypanosomes
o Causes African sleeping sickness
o Trypanosomea brucei
o Symptoms: fever, rashes, parasites enter the central nervous system
causing lethargy and coma
Fatal if not treated
o Predominant in rural areas
o Insect host is tsetse fly in salivary glands -> bites mammalian host, injected
into bloodstream -> parasite multiplies
o Extracellular parasite
o IgG response and complement has lytic activity against trypanosome
o Evades immune system by variant surface glycoprotein VSG
-homogenous
-only antigenic structure at parasites surface
-only one VSG gene is expressed at a time
-superb recombination
-switches expression of VSG genes
-antigenic diversity
Malaria
o Caused by Plasmodium
o Symptoms: recurrent fever, chills, anaemia, cerebral malaria, coma
o Only ~1% cases are fatal
o Life cycle: sexual stage in mosquito -> sporozoites injected into blood (can
hide for years), enters hepatocytes -> asexual liver stage -> merozoited
released into blood stream, asexual stage
o All disease occurs in blood stage
o Immunity develops slowly, is incomplete and declines rapidly
o CTLs can be effective against liver stage (not affective against parasitised
RBCs because no MHC)
o Predominantly antibody mediated
o Mechanism that controls infection is splenic clearance;
-white pulp comprised of lymphocytes, DCs and macrophages
-red pulp contains aged erythrocytes phagocytosed by macrophages ->
removing parasitised RBC from circulation and destroying the parasite
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Parasite: organism that lives/feeds off another organism (host) without providing any benefit to the host. The immune system fights extracellular pathogens by antibodies that opsonise and label pathogens with igg that are recognised by fc receptors on phagocytes (activates phagocytosis): antibodies also activate complement that can lyse extracellular pathogens and also opsonisation. Intracellular pathogens: th1 cells activate macrophages via cytokine ifng and surface molecule cd40l macrophages -> activate respiratory burst -> secrete pro-inflammatory cytokines (tnf, il-1, Il-12) -> upregulating mhc and costimulatory molecules: cytotoxic: recognise peptide on mhc i and kill effector cells by release of cytotoxic granules that contain perforin and granzymes, antibodies play no role in intracellular pathogens but can neutralise. Trypanosomes: causes african sleeping sickness, trypanosomea brucei, symptoms: fever, rashes, parasites enter the central nervous system causing lethargy and coma. Fatal if not treated: predominant in rural areas.
