IMMUNE RESPONSE IN PARASITIC DISEASES

B LO C K M P T 2 0 1 4
10/16/15

Even Semester 2014

non-genetic
Innate immune
system
genetic
IMMUNE
SYSTEM
humoral
Adaptive immune
system
celluler

Multicellular : Helminths
Unicellular : Protozoa

PA
RA
SI
TE

10/16/15

Intracellular : Plasmodium
Extracellular: Entamoeba,
Giardia lamblia
Large size : antigens >>
Multi stage : variation of
antigens
Even Semester 2014

PARASITE INFECTION:
complex multistage life cycles &
involve several hosts.
Route of infection can differ from
oral to penetrate through the skin
directly (hookworm) or by
infectious bites of vector ( malaria)
Many parasites are long-lived and
cause chronic infections.

 The immune response that develops

often proceeds to cause pathologic
changes.

10/16/15

Even Semester 2014

PARASITE SURVIVAL STRATEGIES

Locations:
live in a cyst: Toxoplasma and larva
T.spiralis live in the muscle cyst

Intracellular: Plasmodium
Migration : Hookworm move to escape the
reaction of inflammation

10/16/15

Even Semester 2014

HOOKWORM INFECTION

10/16/15

Even Semester 2014

PARASITE SURVIVAL STRATEGIES

Antigenic variation
Mimicry ( mimicking host antigens)
Produced soluble antigen
Supression regulatory environment: Produced
immunomodulator toxins: Leishmania
produce anti-oxidase
the infected macrophages
10/16/15

Even Semester 2014

inhibit IL-12 by

 Antigenic variation:
VSG (variant surface glycoprotein ) is a
surface molecules which cover the
entire surface of Trypanosoma
gambiense / T. rhodesiense (African
Sleeping sickness)

10/16/15

Even Semester 2014

MICHAEL F. GOOD
NATURE 400, 25-26(1 JULY 1999)

ACUTE AND CHRONIC CONDITIONS

10/16/15

Even Semester 2014

RESPONSE TO HELMINTHS
Multicellular : couldnt be
phagocyte
exist in different stages :
eggs, larvae, adult
Variation of surface antigens
Independently triggered host
immune response
Difficult to eliminate

RESPONSE TO HELMINTHS

Induced both humoral and

cellular response
immunity against helminthic
infections is mediated by Th2
cells, mast cells / basophils
Effector mechanism are
eosinophil and produced Ig E

10/16/15

Even Semester 2014

RESPONSE TO HELMINTHS
In schistosomiasis and filariasis ,
induced Th1 and Th2
Schstosomiasis : in early infection,
dominant induced Th1.
After the worm laying eggs :
induced Th2 cell (antigen release is
omega 1 , a glycoprotein +
ribonucleic acid activity)

SCHISTOSOMIASIS:
STIMULATION OF TH1, EGGS : STIMULATION OF TH2

release omega 1

10/16/15

CD4 Th2 cell ,IL-13,

Macrophage, eosinophil

Even Semester 2014

OUT COMES ASSOCIATED WITH SPECIFIC

IMMUNE RESPONSE TO FILARIA

The presence of Wolbachia (endo

symbiotic bacteria) induce Th1 and Th2
cell
Wolbachia induced pro-inflamary cytokine
IL-6 , TNF, macrophage and chemotactic
activity by neutrophils

10/16/15

Even Semester 2014

OUT COMES ASSOCIATED WITH SPECIFIC

IMMUNE RESPONSE TO FILARIA

10/16/15

Even Semester 2014

IMMUNITY TO PROTOZOA

immunity against intracellular

protozoa is principally mediated
by Th1-triggered macrophages

10/16/15

Even Semester 2014

IN TOXOPLASMOSIS:

10/16/15

Even Semester 2014

IMMUNITY TO MALARIA:

INNATE IMMUNITY

Genetic (associated with human red

blood cells ):
Persons who are negative for the Duffy
blood group are resistant to infection by
P. vivax.
People with thalassemia heterozygote
relatively resistance to malaria infection
((50% reduction in infection),

INNATE IMMUNITY TO MALARIA:

( GENETIC)

sickle cell trait (heterozygotes for the

abnormal hemoglobin gene HbS) are
relatively protected against P. falciparum
(90% protection) and confer protection
against severe malaria and related
mortality
G6PD deficiency, are thought to provide
protection from malaria disease (50%
protection).

INNATE IMMUNITY TO MALARIA:

( GENETIC)

People with Southeast Asian Ovalocytosis

(SAO) relatively resistant to P. falciparum
and P. vivax infections.

10/16/15

Even Semester 2014

ADAPTIVE IMMUNITY
Plasmodium falciparum variant surface
antigen P. falciparum erythrocyte
membrane protein 1 (PfEMP1) is a key
component of clinical immunity against
falciparum malaria.

10/16/15

Even Semester 2014

10/16/15

Even Semester 2014

10/16/15

Even Semester 2014

IMMUNE RESPONSE :
Not always protected
Reinfection in Plasmodium,
Ascaris infection
Not always beneficiary:
Immunopathology Response

Serological test for diagnosis

Make vaccines: Malaria
10/16/15

Even Semester 2014

 Ag-Ab immune
complex in malaria :
glomerulonephritis
P. falciparum infection:
parasitized red blood
cells adhere to the
cerebral capillary
(Cerebral malaria)

IMMUNE RESPONSE (CONTD)

Chronic Amebiasis : formation of
granuloma surrounding the amebic
ulcer (ameboma / amebic granuloma)
Cardiomyopathy in Chagas disease
( Trypanosoma cruzi infection) :
autoimmune reaction to the nerve
ganglion

 Onchocercosis :
Auto immune response to microfilaria
of Onchocerva volvulus produce
blindness

Response granulomatous to eggs

of Schistosoma in liver
cirrhosis

MALARIA
VACCINE
CSP(circumsporozoit protein)
LSA (liver stage antigen)

Pfs 28 & Pfs 25

10/16/15

MSP (merozoite surface protein)

RESA (ring infected surface antigen

Even Semester 2014