respon imun terhadap parasit
DESCRIPTION
imunologiTRANSCRIPT
4/3/2013 [email protected]
The cartoon illustrates the threat to the body from various pathogens (viruses, bacteria, parasites, worms) and the various types of immune responses. The illustration shows leucocytes, which are killing worms, B cells (‘bombers’) which form specific antibodies that destroy bacteria, and cytotoxic T cells (‘police with truncheons’), which destroy virus-infected cells. (© Eric Reits) 4/3/2013 [email protected]
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Adaptive immunity
Innate immunity
Humoral Immune response
Cellular Immune response
Mucosal Immune response
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Antigen E. histolitica
20-32 componentSolubleUn-soluble
Surface :12 glycoprotein strong hydrophobicattachment
Somatic
The triad :Gal–lectin, cysteine proteinases and amoebapores major
proteins involved in the pathogenesis of amoebiasis.
Other amoebic molecules:lipophosphopeptidoglycan, perioxiredoxin, arginase, and lysine and glutamicacid-rich proteins are also implicated
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Attachment
Amoeba’s surface Ag bind to fibronectin & Laminin
Lectin
Matrix extracell:
- Collagen
- Fibronectin
- Laminin
Attachment & Migration into solid tissue
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Surface Ag:-Lectin-Cystein proteinase-Amebaphore
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RELM-β: Resistin like mol β homeostatis of GI & inflamation; TFF3: Trefoil factor Family 3 parameter fungsi sel goblet
Amoebacysteineproteases manipulate and destroy host defences to facilitate nutrient acquisition, parasite colonization and/or invasion.
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Cysteine proteases of the protozoan parasite Entamoebahistolytica are key virulence factors involved in overcoming host defences. These proteases are cathepsin-like enzymes with a cathepsin-L like structure, but cathepsin-B substrate specificity.
In the host intestine, amoeba cysteine proteases cleave colonic mucins and degrade secretory immunoglobulin (Ig) A and IgG rendering them ineffective.
They also act on epithelial tight junctions and degrade the extracellular matrix to promote cell death.
They are involved in the destruction of red blood cells and the evasion of neutrophils and macrophages and they activate pro-inflammatory cytokines IL-1b and IL-18.
Strategies to inhibit the activity of amoeba cysteineproteases could contribute significantly to host protection against E. histolytica. [email protected]
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Lytic activity
Combined chemical & mechanical action:
◦ Chemotaxis
◦ Adhesion
◦ Cytolysis following contact
◦ Phagocytosis
◦ Intracellular degradation
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Chemotaxis:
Locomotion toward target cells
Contact/ adhesion Lysis of target cells
Liberation of enzym & Toxins of amoeba
Intracellular Degradation
Amoeba :- ingest lysed cells
- engulf living cells (RBC)
Nonpathogen : lose their erythrophagocytic activity
(Entamoeba dispar similar morphology, distinc pathogenicity) 4/3
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Inhibition of colonic epithelial cell functions by E. histolytica.(A) Soluble amoebic proteins activate HSF-1 in epithelial cells causing it to trimerize. Activation of HSF-1 induces expression of Hsp 27 and Hsp 72. (B) Increased levels of Hsp 72 have anti-apoptotic effects and lead to increased enterocyte survival. (C) Hsp 27 becomes phosphorylated and associates with IKK, inhibiting its activity and suppressing nuclear factor-κB activation induced by proinflammatory cytokines (IL-1, TNF) released in response to amoebic invasion.HSF = Heat shock protein transcription factor; Hsp = Heat shock [email protected]
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Antibody respons
Intestinal
Circulating
Rapid
1week
IgA/ IgM/ IgG
-Diagnostic Value ELISA
-No Protective Value
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Antibody in Amebiasis
Ab against surface Ag
-Immobilization
Shedding of
Ag-Ab complex
Resistance to Complement lysis
Evade HumoralImmune response
Ab against lectin :
-inhibit adhesion Reduce Cytophatic Effect
-phagocytosis (+)
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Proposed model of IgA-based protection against intestinal infection of E. histolitica
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The life cycle of the malaria parasite Plasmodium falciparumand acquisition of immunity in an area of endemic transmission.
Jean Langhorne, Francis M Ndungu, Anne-Marit Sponaas & Kevin Marsh
Nature Immunology 9, 725 - 732 (2008) doi:10.1038/ni.f.205
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Ab
Ab
Ab
MALARIA
Change over time of various indices of malaria in a population living in an endemic area of P. falciparumtransmission: asymptomatic infection (pink), mild disease (febrile episodes caused by malaria; blue) and severe or life-threatening disease (green). The data are normalized and are presented as the percent of maximum cases for each population index.
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Clinical manifestation of malaria in relation to host immunity in endemic area
Type of vaccines could be used in each specific stage of the parasite's life cycle.
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Vaccine against malaria
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BRADIZOITE FORMATION
Immunocompetent host : CMI cyst
formation
Slow rate bradiz tachiz control by
RNI
To combat intestinal worms, mammals rely on adaptive immune responses mediated by T cells. However, it seems that, initially, innate immune cells mimic T-cell activity, while T cells get ready for action.
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Immune Response againstIntestinal Nematode
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The intestinal epithelium: sensors to effectors in nematode infectionD Artis and R K Grencis
TLSP: Tymic Stromal Prot. Mucosal Immunology (2008) 1, 252–264; doi:10.1038/mi.2008.2
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parasite-specific CD4 T-cell responses elicit nonspecific "modular" type-2 responses
Antibody-coated target cells (i.e: worm) can be killed by NK cells in Antibody Dependent cell-mediated Cytotoxicity (ADCC)
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Hypersensitivity reactions are mediated by immunological mechanism that cause tissue damage
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Arthropod’s Venom:
