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Immunological Aspects of Immunological Aspects of Infectious DiseaseInfectious Disease(Fungi & Parasite)(Fungi & Parasite)
Kuliah Imun Infeksi-LEF
Dr. dr. Dr. dr. LoekiLoeki EnggarEnggar FitriFitri MKesMKes. . SpParKSpParK
1.1. IntroductionIntroduction2.2. Component of the immune systemComponent of the immune system3.3. Non specific iNon specific immunitymmunity to bacteria, to bacteria,
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3.3. Non specific iNon specific immunitymmunity to bacteria, to bacteria, virus, fungi & parasite virus, fungi & parasite
4.4. Specific iSpecific immunitymmunity to bacteria, virus, to bacteria, virus, fungi & parasitefungi & parasite
5.5. Immune evasion of FungiImmune evasion of Fungi6.6. Immune evasion of parasiteImmune evasion of parasite
IntroductionIntroduction
-- The mechanism underlying specific The mechanism underlying specific immunity to many microimmunity to many micro--organism organism remain unknowremain unknow
-- While the immune response has While the immune response has
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-- While the immune response has While the immune response has evolved to confer protection against evolved to confer protection against invading antigens invading antigens human human pathology arisespathology arises
IntroductionIntroduction-- Protective immunity to particular Protective immunity to particular tropical parasitic infection is tropical parasitic infection is frequenlyfrequenly inadequate/noninadequate/non--existentexistent prospect to vaccinationprospect to vaccination
-- People afflicted with tropical People afflicted with tropical
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-- People afflicted with tropical People afflicted with tropical infections often suffer a general infections often suffer a general immunodeficiencyimmunodeficiency
-- Immune responses to tropical Immune responses to tropical infections infections help in diagnosis and help in diagnosis and management management
ImmunopathologicalImmunopathological consequences of consequences of tropical infectionstropical infections
Hypersensitivity typeHypersensitivity type Mechanism Mechanism involvedinvolved
ExamplesExamples
Type I (allergic)Type I (allergic) IgEIgE Lung ascariasisLung ascariasis
Type II (antibodyType II (antibody-- IgGIgG Malaria anaemiaMalaria anaemia
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Type II (antibodyType II (antibody--mediated)mediated)
IgGIgG
AutoantibodyAutoantibody
Malaria anaemiaMalaria anaemia
Streptococci (RHD)Streptococci (RHD)
Type III (immune Type III (immune complex)complex)
Type IV (cellType IV (cell--mediated)mediated)
immune immune complexescomplexes
MacrophagesMacrophages
Malaria kidneyMalaria kidney
Tuberculoid Tuberculoid LeprosyLeprosy
Component of the immune systemComponent of the immune system
The nThe non speon speccifiific immune systemc immune system::--External barriers (skin, mucosalExternal barriers (skin, mucosalsurfaces, flushing mechanism, normalsurfaces, flushing mechanism, normalmicrobial flora)microbial flora)
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microbial flora)microbial flora)--Innate immune system (phagocyte Innate immune system (phagocyte cells,soluble factors & complement)cells,soluble factors & complement)
The The spespeccifiific immune system/acquired c immune system/acquired immune responseimmune response ::
--HHumoral umoral immune responseimmune response--CellCell--mediated immune responsemediated immune response
Non specific iNon specific immunitymmunity to bacteria, virus to bacteria, virus , fungi & parasite, fungi & parasite--The skin The skin is the most important is the most important barrier to invading microorganismbarrier to invading microorganism: : a. secretes sebuma. secretes sebum inhibits inhibits
growth of growth of microorganismmicroorganism..
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growth of growth of microorganismmicroorganism..b. Normal microflora b. Normal microflora competecompete
with pathogenic organismswith pathogenic organisms-- A & b A & b colonization inhibitioncolonization inhibition
3. Non specific i3. Non specific immunitymmunity to bacteria, to bacteria, virus, fungi & parasitevirus, fungi & parasite
--Mucosal surfaces mechanism:Mucosal surfaces mechanism:a.Cilliary movementa.Cilliary movementb.Surface phagocyteb.Surface phagocytec.Enzyme & surface antibody (c.Enzyme & surface antibody (secretory IgAsecretory IgA))d.Mechanical washing by tears or urined.Mechanical washing by tears or urine
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d.Mechanical washing by tears or urined.Mechanical washing by tears or urinee.Obligate aerobs produce potent inhibitors of e.Obligate aerobs produce potent inhibitors of bacterial growth (bacterial growth (BactericinsBactericins) )
f. Obligate anaerobs produce f. Obligate anaerobs produce free fatty acidsfree fatty acidsenvironment less supportive to environment less supportive to microorganismmicroorganism
Non specific iNon specific immunitymmunity to bacteria, virus, to bacteria, virus, fungi & parasitefungi & parasite
Pathogen
PHAGOCYTICCELL
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Lysosomecontainingenzymes
Phagosome
Cellular Innate DefensesCellular Innate Defenses Pathogens entering Pathogens entering
the mammalian the mammalian body are subject body are subject to to phagocytosisphagocytosis
PHAGOCYTICCELL
EXTRACELLULARFLUID Lipopolysaccharide
Helperprotein TLR4
TLR5
Flagellin
to to phagocytosisphagocytosis PhagocyticPhagocytic cells cells
recognize groups recognize groups of pathogens by of pathogens by TLRsTLRs, , TollToll--like like receptorsreceptors
© 2011 Pearson Education, Inc.
TLR9
TLR3
Innate immuneresponses
VESICLE
Non specific iNon specific immunitymmunity to bacteria, virus, fungi & parasiteto bacteria, virus, fungi & parasite
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Evasion of killing Evasion of killing phagocyticphagocytic cells by cells by microorganismmicroorganism
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Chronic InfectionChronic InfectionReRe--activationactivationCarrier stateCarrier state
CoCo--factor for development of certain factor for development of certain malignancymalignancy
Specific iSpecific immunitymmunity to bacteria, virus, fungi & to bacteria, virus, fungi & parasiteparasite
-- Extracellular AgExtracellular Ag induce induce hhumoral umoral immune immune responseresponse
-- Intracellular Ag Intracellular Ag induce cellularinduce cellular immune responseimmune response
The Ags that are capable to bind on The Ags that are capable to bind on specific surface immunoglobulin of B specific surface immunoglobulin of B lymphocyte and induce antibody lymphocyte and induce antibody
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lymphocyte and induce antibody lymphocyte and induce antibody production are referred to as production are referred to as TT--cellcell--independent Ags (figure)independent Ags (figure)
Specific iSpecific immunitymmunity to bacteria, virus & parasiteto bacteria, virus & parasite
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Specific iSpecific immunitymmunity to to IntarcellularIntarcellular bacteria, virus bacteria, virus & parasite& parasite
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MycosesMycoses: diseases caused by fungi: diseases caused by fungi
Asthma and allergyAsthma and allergy Skin diseaseSkin disease
cutaneouscutaneous subcutaneous subcutaneous
Recurrent Recurrent vulvovaginalvulvovaginalcandidiasiscandidiasis
Inflammatory Bowel Inflammatory Bowel DiseaseDisease
Invasive Fungal Disease Invasive Fungal Disease
Superficial MycosesSuperficial Mycoses
TineaTinea ((PityriasisPityriasis) ) versicolorversicolor----pigmented lesions on torsopigmented lesions on torso
TineaTinea nigranigra----gray to black gray to black macular lesions often on palmsmacular lesions often on palms
Black Black piedrapiedra----dark gritty dark gritty deposits on hairdeposits on hairdeposits on hairdeposits on hair
White White piedrapiedra----soft whitish soft whitish granules along hair shaftgranules along hair shaft
Often associated with organisms Often associated with organisms of the genus of the genus MalasseziaMalassezia
All are diagnosed by microscopy All are diagnosed by microscopy and are easily treated by topical and are easily treated by topical preparations.preparations.
CutaneousCutaneous MycosesMycosesThree genera of dermatophytes, Microsporum, Trichophyton, and Epidermophyton cause infections of skin and its appendages.
Clinical Name Site Most frequent organismTinea capitis(epidemic) scalp Trichophyton tonsorus, Microsporum audouinii(epidemic) scalp Trichophyton tonsorus, Microsporum audouiniiTinea capitis (non-epidemic) scalp
Microsporidium canis, Trichophytonverrucosum
Tinea favosa scalp, torso Trichophyton sp.Tinea barbae beard Trichophyton rubrum, T. verrucosum
Tinea coporisarms, legs torso T. rubrum, M. canis, T. mentagrophytes
Tinea cruris crotchT. rubrum, T. mentagrophytes, Epidermophyton floccosum
Tinea pedis, manus feet hands T. rubrum, T. mentagrophytesTinea unguium nails T. rubrum, T. mentagrophytes, E. floccosumTinea imbricata torso T. concentricum
Systemic fungal disease is most often Systemic fungal disease is most often associated with four organismsassociated with four organisms
1.1. CoccidioidesCoccidioides immitisimmitis
SystemicSystemic MycosesMycoses
1.1. CoccidioidesCoccidioides immitisimmitis2. 2. HistoplasmaHistoplasma capsulatumcapsulatum3.3. BlastomycesBlastomyces dermatitidisdermatitidis4.4. ParacoccidioidesParacoccidioides brasiliensisbrasiliensis (S. America)(S. America)
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Immune Response to Fungal InfectionImmune Response to Fungal InfectionEpithelial cells recognize Epithelial cells recognize pathogen associated pathogen associated molecular patterns (PAMPs) molecular patterns (PAMPs) such as such as glucansglucans, , mannansmannans and and chitin.chitin.
In response they secrete In response they secrete In response they secrete In response they secrete cytokines and cytokines and chemokineschemokines to to attract PMNs which provide a attract PMNs which provide a first line of defense.first line of defense.
Natural immunity is highNatural immunity is high; ; physiologic barriers include physiologic barriers include Tissue temperatureTissue temperature----fungi grow fungi grow better at less than 37better at less than 37°°C and C and Secretion of antimicrobial Secretion of antimicrobial peptidespeptides
Pathogen Splinter
Mast
Macro-phage
Signalingmolecules
Movementof fluid
Cellular Innate Defenses To FungiCellular Innate Defenses To Fungi
Mastcell
Capillary
Redblood cells
Neutrophil
molecules
Phagocytosis
Activated neutrophils are critical in the defense against disseminated candidiasis and aspergillosis
Specific Immune Response to Fungal Specific Immune Response to Fungal InfectionInfection
The uptake of fungi by DCs promotes differentiation of T-helper cells.
A dominant TH1 response correlates with protective immunity to fungal infectionsimmunity to fungal infections.Cell-mediated immunity predominates in protectionagainst cryptococcosis, histoplasmosis and mucosal C. albicans infection
IMMUNE RESPONSES TO FUNGIIMMUNE RESPONSES TO FUNGI
Virulence factors help pathogenic fungi Virulence factors help pathogenic fungi to to evade host response and subvert evade host response and subvert basic immune processes basic immune processes basic immune processes basic immune processes
Evasion of the immune responseEvasion of the immune response: yeast : yeast to to hyphalhyphal transition; changing of transition; changing of surface surface glycoproteinsglycoproteins; ; hydrophobinshydrophobins; ; survival in macrophage.survival in macrophage.
A.A. Immune Response: Immune Response: TT--cell mediated (Thcell mediated (Th--1): 1): ILIL--2, 2, IFNIFN--γγ
B.B. Evasion of Defenses: Evasion of Defenses: Resistant to killing Resistant to killing by phagocytesby phagocytes
Systemic fungal disease Systemic fungal disease CoccidioidomycosisCoccidioidomycosis
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by phagocytesby phagocytes---- protein rich, hydrophobic outer wallprotein rich, hydrophobic outer wall----alkaline halo associated with alkaline halo associated with ureaseurease
E. E. Damage: Damage: secreted secreted proteinasesproteinases break down break down collagen, collagen, elastinelastin, hemoglobin, , hemoglobin, IgGIgG & & IgAIgA
Histoplasmosis(also called (also called cave diseasecave disease))
Caused by the dimorphic fungus Histoplasma capsulatum
Tuberculated macroconidia, grown at 25CIntracellular yeast at 37C
Histoplasmosis is characterized by intracellular growth of the pathogen in macrophages and a granulomatous reaction in tissue.
These granulomatous foci may reactivate and cause dissemination of fungi to other tissues.
HistoplasmosisHistoplasmosis
Immune Response Immune Response 1.1. CellCell--mediated responses are of primary mediated responses are of primary
importanceimportance2.2. PhagocyticPhagocytic activity of macrophage is considered activity of macrophage is considered
an important component of resistance to drugs.an important component of resistance to drugs.Activated macrophage can kill yeast cellsActivated macrophage can kill yeast cells
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3.3. Activated macrophage can kill yeast cellsActivated macrophage can kill yeast cells
Evasion of DefensesEvasion of Defenses1.1. Survival in macrophagesSurvival in macrophages——elevates pH of elevates pH of
phagosomesphagosomes2.2. Yeast cells absorb iron and calcium from hostYeast cells absorb iron and calcium from host3.3. Alteration of cell surface Alteration of cell surface
:
BlastomycesBlastomyces dermatitidisdermatitidis
Evasion of DefensesEvasion of Defenses: : Escapes Escapes phagocytosisphagocytosis by by neutrophilsneutrophils and and monocytesmonocytes by shedding its surface by shedding its surface antigen after infectionantigen after infection
Alveolar macrophage provide a first Alveolar macrophage provide a first Alveolar macrophage provide a first Alveolar macrophage provide a first line of defense.line of defense.
TT--cell stimulated cell stimulated PMNsPMNs kill kill BlastomycesBlastomyces cells (by oxidative cells (by oxidative mechanisms).mechanisms).
Conidia are more sensitive to killing Conidia are more sensitive to killing by by PMNsPMNs because yeast are too big.because yeast are too big.
THTH--1 response of primary 1 response of primary importanceimportance
Opportunistic MycosesOpportunistic Mycoses
Cryptococcus Cryptococcus neoformansneoformansAbout 30% of About 30% of cryptococcuscryptococcus infections occur in patients infections occur in patients
with lymphoma (CNS). Major with lymphoma (CNS). Major oportunisticoportunistic infection in infection in patients with AIDSpatients with AIDSpatients with AIDSpatients with AIDS
Evasion of defensesEvasion of defenses: Yeast cells are resistant to : Yeast cells are resistant to phagocytosisphagocytosis because of capsule. Melanin protects because of capsule. Melanin protects against oxidative injuryagainst oxidative injury
•• Immune responseImmune response: Activated : Activated neutrophilsneutrophils have an have an increased capacity to increased capacity to phagocytizephagocytize C. C. neoformansneoformans. Cell . Cell mediated immunity is mediated immunity is a primary defense. a primary defense.
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CandidiasisCandidiasis
Immune ResponseImmune Response HyphaeHyphae are too big for are too big for phagocytosisphagocytosis but are but are
damaged by damaged by PMNsPMNs and by extracellular mechanisms and by extracellular mechanisms ((myeloperoxidasemyeloperoxidase and and ββ--glucuronidaseglucuronidase). Cytokine ). Cytokine ((myeloperoxidasemyeloperoxidase and and ββ--glucuronidaseglucuronidase). Cytokine ). Cytokine activated lymphocytes can inhibit growth of activated lymphocytes can inhibit growth of C. C. albicansalbicans. .
Resistance to invasive infection by Candida is Resistance to invasive infection by Candida is mediated by mediated by phagocytesphagocytes, complement and antibody, , complement and antibody, and T cell mediated immunity plays a major role. and T cell mediated immunity plays a major role. Patients with defects in Patients with defects in phagocytosisphagocytosis function and function and myeloperoxidasemyeloperoxidase deficiency are at risk for deficiency are at risk for disseminated (even fatal) disseminated (even fatal) CandidiasisCandidiasis. .
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HumoralHumoral immunity (Antibody) to parasiteimmunity (Antibody) to parasite
IgG Malaria
IgM Malaria, Trypanosoma
IgE Extraluminal helminth
IgA Intra Lumenal helminth
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IgA Intra Lumenal helminth
a. a. Lysis by ALysis by Antibodyntibody/complement/complementLysis sporozoite or merozoiteLysis sporozoite or merozoite of of Plasmodium, Plasmodium, LysisTrypanosoma LysisTrypanosoma Lysis extraluminal helminthLysis extraluminal helminth
b. Nb. Neutralizedeutralized by antibody (parasite by antibody (parasite can nocan nolonger gain entry into the cells)longer gain entry into the cells)neutralisingneutralising antibody to santibody to sporozoit or porozoit or merozoite ofmerozoite of PlasmodiumPlasmodium,,Trypanosoma Trypanosoma
cruzycruzy&&Toxoplasma gondiiToxoplasma gondii..
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&&Toxoplasma gondiiToxoplasma gondii..
c. c. Opsonization of MacropOpsonization of MacrophhagesagesPlasmodium dan TrypanosomaPlasmodium dan Trypanosoma..
d. d. Antibody dependent cell mediated Antibody dependent cell mediated cytotoxicity (ADCCcytotoxicity (ADCC))Schistosoma, Trichinella & FilariaSchistosoma, Trichinella & Filaria
Granuloma formationGranuloma formationGranulomaGranuloma form as a consequence of the body’s form as a consequence of the body’s defencedefence mechanism for walling off pathogensmechanism for walling off pathogens
GranulomaGranuloma can be defined as a focal, compact can be defined as a focal, compact collection of inflammatory cells in which collection of inflammatory cells in which mononuclearsmononuclearspredominate and are predominate and are ussuallyussually formed as a result of formed as a result of
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predominate and are predominate and are ussuallyussually formed as a result of formed as a result of undegradableundegradable or persisting microorganism and are due or persisting microorganism and are due to Delayed Type Hypersensitivity (to Delayed Type Hypersensitivity (DTHDTH).).
GranulomaGranuloma is an active site of numerous enzymes and is an active site of numerous enzymes and cytokinescytokines
Intraluminal helminth:Intraluminal helminth:
Most Most helminthhelminth extracellular & too large for extracellular & too large for phagocytosisphagocytosis. Some gastrointestinal host . Some gastrointestinal host develops develops inflamationinflamation and hypersensitivity to and hypersensitivity to expel the wormsexpel the worms
The expulsion of some intestinal The expulsion of some intestinal nematodanematodaoccurs spontaneously a few weeks after occurs spontaneously a few weeks after
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occurs spontaneously a few weeks after occurs spontaneously a few weeks after primary infection.primary infection.
There seem to be two stages in the There seem to be two stages in the expulsion which is achieved by a expulsion which is achieved by a combination of Tcombination of T--dependent and Tdependent and T--independent mechanismindependent mechanism
Mekanisme Penghindaran ParasitMekanisme Penghindaran Parasit daridariPengawasanPengawasan SistemSistem ImunImuna. Ukuran parasit yang besara. Ukuran parasit yang besar
Sulit untuk sistem imun mengeliminasi parasit Sulit untuk sistem imun mengeliminasi parasit dengan ukuran besar. Respon imun pertama dengan ukuran besar. Respon imun pertama adalah inflamsi untuk inisiasi ekspulsi, tetapi adalah inflamsi untuk inisiasi ekspulsi, tetapi kebanyakan cacing tetap tidak bisa dikeluarkankebanyakan cacing tetap tidak bisa dikeluarkan..
b. b. Keragaman antigenikKeragaman antigenikParasit Parasit beberapa stadium beberapa stadium tiap stadium cocok tiap stadium cocok
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b. b. Keragaman antigenikKeragaman antigenikParasit Parasit beberapa stadium beberapa stadium tiap stadium cocok tiap stadium cocok dengan Ab tertentudengan Ab tertentumismis: : Plasmodium Plasmodium IgG penderita daerah endemis IgG penderita daerah endemis
efek terapeutikefek terapeutik
African TrypanosomesAfrican Trypanosomesmempunyai suatu glikoprotein mempunyai suatu glikoprotein menutup permukaan tubuh. menutup permukaan tubuh. Protein yang bersifat imunodominan ini Protein yang bersifat imunodominan ini disebut disebut variant surface glycoproteinsvariant surface glycoproteins(VSG) (VSG)
Gen yang mengkode protein ini adalah Gen yang mengkode protein ini adalah suatu “gene cassettes” yang menyebabkan suatu “gene cassettes” yang menyebabkan VSG dapatVSG dapat switchswitch secara reguler menjadi secara reguler menjadi VSG dengan tipe yang berbeda. VSG dengan tipe yang berbeda.
Ab. VSG tertentu tidak dapat digunakan Ab. VSG tertentu tidak dapat digunakan untuk VSG tipe lain untuk VSG tipe lain parasit tak dikenal parasit tak dikenal oleh hospesoleh hospes..
c. c. Belajar hidup dalam MakrofagBelajar hidup dalam Makrofaguuntuk ntuk ParParasit asit IntraselIntrasel, , mis: Toxoplasmamis: Toxoplasma,,TrypanosomaTrypanosoma,, LeishmaniaLeishmania
Cara:Cara:-- Menggagalkan fusi Lisosom & fagosomMenggagalkan fusi Lisosom & fagosom
mis : Toxoplasma (≈ mis : Toxoplasma (≈ M. TuberculosisM. Tuberculosis))-- Menghindar dari Lisosom Menghindar dari Lisosom cytoplasmacytoplasma
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-- Menghindar dari Lisosom Menghindar dari Lisosom cytoplasmacytoplasmamis : Trypanosomamis : Trypanosoma
-- Menyelimuti diri atau membentuk kapsul pelindung Menyelimuti diri atau membentuk kapsul pelindung tahan thd pengaruh lisosomtahan thd pengaruh lisosom
mis : Leishmania (mis : Leishmania (≈ ≈ M Tuberculosa, M LepraM Tuberculosa, M Lepra))
dd. . Supresi tanggap kebalSupresi tanggap kebalParasit merusak sel dan jaringan Parasit merusak sel dan jaringan limfoid, dengan cara limfoid, dengan cara : : 1. M1. Mengeluarkan engeluarkan bbahanahan sitotoksiksitotoksik: :
-- merusak jar. Limfoid merusak jar. Limfoid
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-- memecah molekul IgGmemecah molekul IgG
2. 2. Melepaskan antigen dalam jumlah besar Melepaskan antigen dalam jumlah besar mengganggu respon imun, dengan :mengganggu respon imun, dengan :
-- Mengikat Ab Mengikat Ab tdk mencapai parasittdk mencapai parasit-- Memblok sel efektorMemblok sel efektor langsung (Tc)langsung (Tc) Membentuk kompleks immun (sel K/ADCC)Membentuk kompleks immun (sel K/ADCC)
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Membentuk kompleks immun (sel K/ADCC)Membentuk kompleks immun (sel K/ADCC)-- Menginduksi toleransi sel B dan T thd parasitMenginduksi toleransi sel B dan T thd parasit-- Aktivasi Poliklonal Aktivasi Poliklonal pelepasan bahan bahan pelepasan bahan bahan mitogenik mitogenik Ab >> non spesifik Ab >> non spesifik
-- Aktivasi sel supresorAktivasi sel supresor
ee. Subversi tanggap kebal, merubah sifat. Subversi tanggap kebal, merubah sifat salah salah satu komponen sistem imunsatu komponen sistem imunContoh: Cestoda Contoh: Cestoda Proteoglycan Proteoglycan
Inaktivasi komplemenInaktivasi komplemenf. f. AntiAnti--immune mechanismimmune mechanism
Leishmania memproduksi antiLeishmania memproduksi anti--oxidases untuk oxidases untuk
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Leishmania memproduksi antiLeishmania memproduksi anti--oxidases untuk oxidases untuk menetralisir produksi radikal bebas dari menetralisir produksi radikal bebas dari macrophag yang teraktivasimacrophag yang teraktivasi
g. g. Penyamaran antigenik Penyamaran antigenik Parasit menggunakan Ag Parasit menggunakan Ag inanginang mantelmantelmis: Schistosomamis: Schistosoma
Schistosoma mengambil protein darah inang, Schistosoma mengambil protein darah inang, seperti seperti blood group antigensblood group antigens & molekul MHC & molekul MHC class I & II , akibatnya, cacing bersifat class I & II , akibatnya, cacing bersifat “self”. “self”. class I & II , akibatnya, cacing bersifat class I & II , akibatnya, cacing bersifat “self”. “self”.
Tegumen cacing cestode & trematode , Tegumen cacing cestode & trematode , dapat mengabsorbsi komponen inang, misal. dapat mengabsorbsi komponen inang, misal. Antigen eritrosit. Hal ini menyebabkan Antigen eritrosit. Hal ini menyebabkan cacing secara imunologis sama dengan inang. cacing secara imunologis sama dengan inang.
Evasion strategies ofEvasion strategies ofectoparasites of vertebratesectoparasites of vertebrates..
Ectoparasites juga mempunyai strategi untukEctoparasites juga mempunyai strategi untukmenghindari pertahanan inang tapi bukan suatumenghindari pertahanan inang tapi bukan suatuimmun evasionimmun evasion.. Rapid feedingRapid feeding of bloodof blood--sucking insects to sucking insects to Rapid feedingRapid feeding of bloodof blood--sucking insects to sucking insects to
avoid host defensive movements.avoid host defensive movements. Use of ‘hooks/claws’Use of ‘hooks/claws’ e.g. claws on tarsi of e.g. claws on tarsi of
head lice etc. used to hold on to hair head lice etc. used to hold on to hair –– allows allows parasite to survive grooming activities of parasite to survive grooming activities of host.host.