Blok Immune Mpt 131

8/12/2019 Blok Immune Mpt 131

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IMMUNO-PARASITOLGY

Immune Response and Immuno-diagnosis

In Parasitic Diseases
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non-genetic

Innate immunesystem

genetic

IMMUNESYSTEM

humoral

Adaptive immunesystem

celluler
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Parasite :

Multicellular : Helminths

Unicellular : Protozoa

Intracellular : Plasmodium

Extracellular : Entamoeba

Large size : antigens >>

Multi stage : variation of antigens
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Parasite infection:

Have complex multistage life

cyclesthat 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.


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Parasite infection(contd)

chronic parasite-infections are

common owing to weak innate

immunity and parasite capacity to

evade the immune response

The immune response that

develops often proceedsto cause

pathologic changes.


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Parasite survival Strategies

Locations: Paragonimus live in a cyst in the

lung ,

Toxoplasma and larva T.spiralislive in the muscle cyst,

Plasmodium live inside the redblood cell

Migration : Hookworn (A. duodenale)move to escape the reaction ofinflammation


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Parasite survival (contd)

Antigenic variation:

VSG (variant surface

glycoprotein ) is a surface

molecules which cover the entire

surface of Trypanosoma

gambiense / T. rhodesiense

(African Sleeping sickness)


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Parasite survival (contd)

Mimicry ( mimicking host antigens) ,ex: Schistosoma

Produced soluble antigen :

depressed the immune response(ex: lymphocytotoxic fc )

Produced immunomodulator toxins:

Leishmania produce anti-oxidaseinhibit IL-12 by the infectedmacrophages
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Response to Helminths

Multicellular: couldnt bephagocyte

exist in different stages : eggs,

larvae, adult Variation of surface antigens

Independently triggered host

immune response

Difficult to eliminate


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Response to helminths(contd)

Induced both humoral andcellular response

immunity against helminthic

infections is mediated by Th2cells, mast cells / basophils

Effector mechanism are

eosinophiland produced Ig E
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Secreted immunomodulators : e.g.

cysteine protease inhibitors

(cystatins)

Inhibit antigen processing and

presentation

reduce T cell responses


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Exception :

In schistosomiasis and filariasis ,

induced Th1 and Th2

Schstosomiasis : in early infection,dominant induced Th1.

After the worm laying eggs :

induced Th2 cell (antigen releaseis omega 1 , a glycoprotein +

ribonucleic acid activity)


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Formation of granuloma:

Eggs that trapped in the tissue

release omega 1CD4 Th2 cell ,IL-13,

Macrophage, eosinophil

granuloma

fibrosis of the liver


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Filariasis :

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


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Out comes associated with specific immune

response to Filaria


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Immunity to Protozoa

immunity against intracellular

protozoa is principally mediated

by Th1-triggered macrophages


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Innate immunity in Malaria

Genetic :

Play role in early infection:

malaria

RBC membrane disorder:

Antigen Duffy : a receptor forP. vivax.

People with Ag Duffy (-) moreresistant P. vivax infection


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Innate immunity((contd)

Glycophorine A: receptor for P.falciparum more resistant

toP. falciparum infectionOvalocytocis

Disorder of band3

protein, more resistant to P.vivax, P. malariae andP.falciparum


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Erythrocyte disorder

G-6-PD deficiency : patients moreresistant to P. falciparum

Haemoglobinopathy: condition of

RBC influence the life ofPlasmodium:

Sickle cell anemia

Thalasemia Hb -F; Hb- C; Hb-D; Hb-E


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Non genetic

Hormone: pregnant woman

easier to have complicated

malaria


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Immunity to Plasmodium

The Plasmodium exists in

humans in :

extracellular forms: sporozoitesand merozoites,

intracellular stages in

hepatocytes and erythrocytes.


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Its stimulates CD4 and CD8 T

cells, gamma-delta T cells,

macrophages, natural killer(NK) cells, and B cells

make antibodies against

epitopes : on the surface of the sporozoite,

merozoites


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Ab helping macrophage tophagocyte Trypanosome


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In toxoplasmosis


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Response to Intestinal protozoa

Gut Associated Lymphoid tissue(GALT)

Mucosal lymphoid follicles

Immunological active cell in thelamina propria

The protozoa stimulate inflammation:

Proliferation, crypt >>, atrophy of thevillous

Malabsorption syndrome

Hypermotility


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Response to intestinal protozoa

infection

Activation of Intraepithelial

lymphocyte, especially CD8+ T

cell Function:

To produce cytokine ( IFN and IL-

10) Cytotoxicity process

Apoptosis and cell regeneration


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Immune response:

Not always protected Reinfection in Plasmodium, Ascaris

infection

Not always beneficiary: Immunopathology Response

Allergic reaction:

anaphylactic shock inhydatidosis

Syndroma Loeffler


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Ag-Ab immune

complex in malaria :

glomerulonephritis

P.falciparum infection:parasitized red blood

cells adhere to the

cerebral capillary(Cerebral malaria)


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Immune response (contd)

Chronic Amebiasis : formation ofgranuloma surrounding the amebic

ulcer (ameboma / amebic

granuloma)

Cardiomyopathy in Chagas

disease ( Trypanosoma cruziinfection) : autoimmune reaction to

the nerve ganglion


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Onchocercosis :

Auto immune response to

microfilaria of Onchocerva

volvulusproduce blindness

Response granulomatous to

eggs of Schistosomain livercirrhosis


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The Advantage of Immune

response :

I. Immuno-diagnosis (sero-diagnosis)

Based on antigen-antibody

reaction

Antibody / antigen detection

When do we need ??

Parasite difficult to find Pre-patent and chronic phase

Light infection (number of parasite


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II. Make vaccines

An ideal malaria vaccine : safe,cheap, easy to manufacture,

easy to administer and confer

life-long immunity against thedisease

Three main types of vaccines,

are being developed:


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1. A pre-erythrocytic /

antisporozoite :

would prevent invasion of

hepatocytes by sporozoites

and/or prevent liver-stage

parasites from developing tomaturity, e.g.:

oCSP ( circum sporozoite

protein)


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2.Againts asexual blood stage

to induce Ab that neutralize/

destroy the merozoites and

infected RBC, and block

cytoadherence,

Proteins identified :

MSP 1 (merozoit surfaceprotein), MSP 2, MSP 3


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Vaccines against asexual

blood (contd)

o apical merozoite surface

antigen 1 (AMA-1),

o the 175 kDa erythrocyte binding

antigen (EBA175)

o and rhoptry- associated protein

1 (RAP-1), RAP-2

o RESA (ring infected

erythrocyte surface antigen)


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3. Blocking transmission

inducing Ab that inactivategametocytes and interfere

with fertilization would

prevent transmission of thedisease.


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Immunocompromised host

some diseases can be dangerousand fatal

Helminths :

Strongyloides stercoralis Cysticercosis

Protozoa:

Toxoplasma gondii Cryptosporidiosis

Cyclospora
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Blok Immune Mpt 131

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