Hipersensitivitas Tipe III Dan IV

8/13/2019 Hipersensitivitas Tipe III Dan IV

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HIPERSENSITIVITAS

TIPE III dan IV


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HYPERSENSITIVITAS

Yaitu : Rx Imun yang patologic,terjadi

akibat respon imun yang

berlebihan sehingga

menimbulkan kerusakan jaringantubuh.

Rx ini dapt terjadi bila :

- Jumlah Ag yang masuk relatif banyak

- Rx tidak pernah timbul pada pemaparan pertama


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Respon Imun yang menimbulkan Penyakit Hipersensitivitas

Respon

Imun

Faktor yang Menguntungkan

Proteksi Terhadap infeksi

Pengendalian pertumbuhan

Pre-Kangker

Alergi

Penyakit Autoimun

Penolakan Graft

Eritroblastosis Fetalis

Faktor yang Tidak Diinginkan


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PEMBAGIAN HIPERSENSITIVITAS MENURUT WAKTU

I. Rx CEPAT

Dalam hitungan detik menghilang dalam waktu 2

jam

Contoh : Anafilaksis sistemikAnafilaksis lokal seperti pilek,

bersin,asma,urtikaria dan eksim


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2. Rx INTERMEDIET

TERJADI SETELAH BEBERAPA JAM DAN

MENGHILANG DALAM 24 JAMManisfestasi dapat berupa :

a. Reaksi tranfusi darah,

Eritroblastosis fetalis

anemia hemolitik autoimunb. Artritis reumatoid,vasculitis necrotis


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3. REAKSI LAMBAT

Reaksi lambat terlihat setelah 48 jam

setelah pajanan dengan antigen

contoh : Dermatitis kontak


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Manifestasi dan mekanisme reaksi

Hipersensitivitas

Tipe Manifestasi Mekanisme

I Reaksi hipersensitivitas cepat Biasanya IgE

II Antibodi terhadap sel IgG atau IgM

III Kompleks antigen-antibodi IgG (terbanyak) / IgM

IV Reaksi hipersensitivitas lambat Sel T yang disensitasi


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Type I

IgE Mediated

Classic Allergy

Type II

IgG/IgM

Mediated

rbc lysis

Type III

IgG Mediated

Immune

complex

Disease

Type IV

T cell

Delayed

Type

Hypersensitivity

Gel and Coombs classification of hypersensitivities.


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4. Hipersensitivitas Tipe IV

- Tipe lambat (24-48 jam )

- Tipe selluler

- Sel limfosit yang telah tersensitisasi bereaksi

secara spesifik dengan suatu antigen tertentu

Rx TuberkulinRx Granuloma


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III. R. Tipe III (R. complex Immune/R. Immunecomp toxic)

Penyebab keracunan / diseaseimmune comp

Pada tipe tsb, baik Ag Ablepas ikatan tsb dapat dibawa ke mana2x

sirkulasitergantung dimana comp tsb tersangkut.

Kalau tersangkut pd ginjalkencing nanah

Kalau tersangkut pd perutbatuk darah

Ag dpt bersal dari : kuman patogen; spora jamur; jaringan sendiri (auto imun)

Ag+Abcomp. Ag-Abikut dlm sirkulasi darahada tempat2x khusus yg

dapt berikatan dengan complemen tersebut.

Kejadian bisa terjadi ikatan mirip R.I atau RII


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IV. R. Tipe Iv (R. Hipersensitivitas lambat)

DTH : delayed Type Hypersensitivity

CMI : Cell Mediated Immunity : Immune cellular

R. tipe IV. Sepintas gambaran mirip immune cellulerakibat yang ditimbulkan

berbeda

Kalau CMImelindungi tubuh

Kalau DTH

merusak tubuh

R. terjadi ok. Sel Ttersensitisasi Ag t3 tidak ada peranan Absel T

melepas sitokin (limfokin) AL : MIF ; MAF

MQ yang teraktifkan kerusakan jaringan

Ag pencetusjaringan asing (virus, mycobacteria)

prot. Asing

bhn kimiamenembus kulit

metal

serbuk bedak


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TYPE III

Immune Complexes

PMNs and macrophages bind to immune complexes via

FcR and phagocytize the complexes.

BUT

If unable to phagocytize the immune complexes can

cause inflammation via C activation ---> C3a C4a, C5a

and "frustrated phagocytes".


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TYPE III

Immune Complex Disease"Frustrated Phagocytes" If neutrophils and macrophages are unable to phagocytize the immune

complexes these cells will degranulate in the area of immune complex

deposition and trigger inflammation.

Unable to eat -------try to digest outside cell.


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TYPE III

Immune Complex Disease

Localized disease

Deposited in joints causing local inflammation = arthritis. Deposited in kidneys = glomerulonephritis.


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TYPE III

Immune Complex Disease

Serum sickness from large amounts of antigen such as injection offoreign serum.

Serum sickness is usually transient immune complex disease

with removal of antigen source.


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Serum Sickness

Systemic immune complex disease

Days after Antigen Injection

Large amounts of antigen

such as injection of

foreign serum.


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Delayed type hypersensitivity

Th1 cells and macrophages

DTH response is from:

Th1 cells release cytokines to activate macrophages causing inflammation

and tissue damage.

Continued macrophage activation can cause chronic inflammation resulting

in tissue lesions, scarring, and granuloma formation.

Delayed is relative because DTH response arise 24-72

hours after exposure rather than within minutes.


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Stages of Type IV DTHEffector stage

Secondary contact yields what we call DTH.

Th1 memory cells are activated and produce cytokines.

IFN-g, TNF-a, and TNF-bwhich cause tissue destruction, inflammation. IL-2 that activates T cells and CTLs.

Chemokines- for macrophage recruitment.

IL-3, GM-CSF for increased monocyte/macrophage


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Stages of Type IV DTHEffector stage

Secondary exposure to antigen

Inflamed area becomes red and fluid filled can form lesion.

From tissue damage there is activation of clotting cascades and tissue repair. Continued exposure to antigen can cause chronic inflammation and result

in granuloma formation.


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Contact dermatitis


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Delayed type hypersensitivity

(DTH)

DTH is a type of immune

response classified by

Th1 and macrophage

activation that results in

tissue damage.

DTH can be the result of

Chronic infection or

Exposure to some antigens


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Granuloma Formation from DTH

Mediated by Chronic Inflammation


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Drug reactions can be any Type

of Hypersensitivity

Hipersensitivitas Tipe III Dan IV

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