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