6.imunologikulit new
DESCRIPTION
definisietiologimanifestasi klinispatofisiologipenatalaksanaanprognosisTRANSCRIPT
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PENGETAHUAN DASAR
IMUNOLOGI KULIT
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Pendahuluan
pengenalan, memori, kespesifikan
terhadap benda asing → inti imunologi
imunologi: ilmu yg mempelajari mengenai
sistem imun
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Sistem Imun
→ gabungan sel, molekul, & jaringan yg
berperan dlm resistensi terhadap infeksi
Respons Imun
→ reaksi yg dikoordinasi sel-sel, molekul-
molekul terhadap mikroba&bahan lainnya
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Perbedaan sifat-sifat sistem imun
nonspesifik dan spesifik Resistensi: tdk berubah
o/infeksi
Spesifitas: efektif thdp semua mikroba
Sel yg penting: fagosit,sel NK,sel mast,eosinofil
Molekul yg penting:
lisozim,komplemen,APP,
interferon,CRP,kolektin,
molekul adhesi
membaik o/infeksi berulang(=memori)
Spesifik u/mikroba yg sdh mensensitasi sebelumnya
Th,Tdth,Tc,Ts,sel B
antibodi,sitokon,mediator,molekul adhesi
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Imunitas
resistensi terhadap penyakit terutama
penyakit infeksi
imunitas nonspesifik & spesifik
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Imunitas Nonspesifik & Spesifik
Imunitas nonspesifik
Positif:
• selalu siap
• respons cepat
• tdk perlu ada pajanan
sebelumnya
Negatif:
• dpt berlebihan
• kekurangan memori
Imunitas spesifik
Negatif:
• tdk siap s/terpajan
• respons lambat
Positif:
• respons intens
• perlindungan lbh baik
pd pajanan berikut
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Respons Imun
Respons imun nonspesifik:
• fagositosis
• peradangan
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2 komponen sistem imun
1. Respons imun humoral:
meliputi globulin-gama tertentu:
imunoglobulin,sebagian merupakan
antibodi spesifik
2. Respons imun selular:
diperankan o/limfosit +
produknya(limfokin) → reaksi
hipersensitivitas tipe lambat
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Respons imun terjadi sbg akibat peristiwa
yg menyangkut antigen,limfosit,antibodi,
limfokin/sitokin,mediator kimia,sel efektor.
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Mediator
Substansi kimia yg mempengaruhi & memacu respons imun & proses peradangan
Komplemen,SRSA,prostaglandin,faktor permeabilitas limfonoduli,protease, fibrinolisin, dll.
Histamin:vasodilatasi,pengeluaran protein,menimbulkan rasa gatal,memacu respons peradangan
Serotonin
Kinin
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Sitokin
sistem komunikasi terintegrasi yg menyebabkan pergerakan & interaksi antar sel.
dinamakan sesuai dgn fungsinya (interferon,TNF,TGF)
1 jenis sitokin dpt mempunyai berbegai fungsi: interleukin → IL-1 sampai IL-18, interferon(membatasi replikasi virus), TNF(proses inflamasi),CSF(kematangan berbagai jenis leukosit),TGF(penghambat suatu proses:inflamasi&penyembuhan luka,kemokin
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Imunitas Humoral
diperankan o/ limfosit B
limfosit B berdiferensiasi menjadi sel
plasma → memproduksi imunoglobulin
5 (lima) imunoglobulin:
IgG,IgA,IgM,IgD,IgE
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Imunitas Selular
diperankan oleh sel T + limfokinnya
imunoglobulin pd permukaan sedikit
sel T → limfokin:
macrophage inhibitory factor (MIF),
macrophage activating factor (MAF),
macrophage chemotactic factor (MCF),
leucocyte inhibitory factor (LIF)
interferon & limfotoksin
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Reaksi Hipersensitivitas
Reaksi imun yg patologik,terjadi akibat
respons imun yg berlebihan shg
menimbulkan kerusakan jaringan tubuh
Reaksi hipersensitivitas,dibagi menurut:
1. waktu terjadinya
2. mekanisme
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Reaksi Hipersensitivitas menurut waktu
Reaksi cepat:terjadi dlm hitungan detik,
menghilang dalam 2 jam
Reaksi intermediate:terjadi setelah
beberapa jam,menghilang dlm 24 jam
Reaksi lambat:terlihat sampai sekitar 48
jam setelah pajanan dgn antigen
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Reaksi Hipersensitivitas menurut
mekanisme (Coombs& Gell)
Reaksi tipe I (reaksi cepat/anafilaksis/ alergi): alergen + IgE → urtikaria
Reaksi tipe II (reaksi sitotoksis/sitolitik):
IgG + IgM dgn antigen yg melekat pd sel
→ pemfigus vulgaris
Reaksi tipe III (reaksi kompleks imun):
agregasi antigen,antibodi,komplemen
→ vaskulitis nekrotikans
Reaksi tipe IV (reaksi alergik seluler tipe lambat): limfosit T,APC,sel Langerhans →
DKA
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Klasifikasi hipersensitivitas oleh Gell dan Coombs
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Hipersensitivitas Type I
Dikenal sebagai :
Immediate
hypersensitivity
Anaphylaxis
IgE-associated
immune
responses
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Hipersensitivitas Type I : Animasi I
Produksi IgE sebagai respons terhadap alergen
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Hipersensitivitas Type I : Animasi II Alergen yang berintegrasi dengan IgE pada
permukaan sel mast memicu pelepasan mediator
inflamasi
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Triggering Phase
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Granule proteins
MBP, ECP, EPO
Cytokines
IL-3, IL-4, IL-5, GM-CSF,
IL-6, IL-12, TGF-b
LTC4, PAF Chemokines
Eotaxin, RANTES
Epithelial damage / loss
Muscarinic M2 dysfunction/ AHR
Attract/activate eosinophils
Airway remodelling, IgE,
Th2 polarisation
Attract/activate eosinophils
Mucus hypersecretion,
Airway narrowing
Attract/activate
pro-inflammatory cells
Products of Human Mast
Cells
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Hipersensitivitas Type I
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Components of Type I
Reactions: 1.
2.
3. 4.
5.
6.
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Anaphylactic-type
Degranulation of a Mast
Cell
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Hipersensitivitas tipe I
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Angioedema
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Dermatitis
Exfoliativa
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Hipersensitivitas Type II
Antibodi IgG dan IgM
Proses imun yang
terjadi : pengaktifan komplemen,dan
terjadi lisis (MAC)
Fagositosis dan lisis via
FcR dan komplemen
receptor
ADCC via NK sel atau
eosinofil
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Hipersensitivitas Type II Antibody-Complement Dependent
Mediated Lysis
Animasi : IgG atau IgM bereaksi dengan epitop pada membran
sel host dan mengaktifkan jalur klasik komplemen. terbentuknya
Membrane Attack Complex (MAC) menyebabkan lisis dari sel
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Hipersensitivitas Type II Antibody-Complement Dependent Mediated
Lysis
Contoh: Autoimmune Hemolytic Anemia
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Animasi: Antibodi bereaksi dengan epitop pada
membran sel host dan NK sel berikatan dengan FC
antibodi. NK sel kemudian melisiskan sel
Hipersensitivitas Type II Antibody Dependent Cell Mediated
Cytotoxicity
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Eritroblastosis foetalis
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Hipersensitivitas Type III
“Immune complex disease”
Proses imun yang
terjadi : Jalur klasik komplemen
Fagositosis
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Hipersensitivitas Type III
Pada umumnya patogenesis kerusakan jaringan oleh kompleks imun tersebut berlangsung dalam 4 tahap :
Terjadi reaksi antibody antigen membentuk kompleks imun
Dalam kondisi tertentu kompleks imun akan mengendap pada jaringan seperti kulit, ginjal dan sendi
Faktor humoral seperti komplemen atau enzim fagosit dan faktor seluler akan berada di daerah pengendapan
Kerusakan jaringan oleh faktor humoral dan seluler
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Hipersensitivitas Type III : Immune
Complex
Animasi: Sejumlah besar kompleks antigen antibodi yang beredar dalam darah
tidak dieliminasi secara komplet oleh makrofag. kompleks antigen antibodi
mengendap di kapiler diantara sel endotel dan membran basalis. kompleks antigen
antibodi mengaktifkan jalur komplemen, yang juga menarik leukosit ke daerah
tersebut. Leukosit kemudian melepaskan agen dan meyebakan terjadinya inflamasi
masif. Ini menyebakan kerusakan dan kematian jaringan
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Hipersensitivitas Type III : Arthus
Reaction
(reaksi lokal)
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Arthus Reaction
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Malar rash
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Rheumatoid Arthritis
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Contoh Hipersensitivitas Type IV
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Peran Limfokin pada DTH
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TH1-mediated Type IV Hypersensitivity
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TH1 Influence of Immune
Response
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DTH Response
Cytokines released include: TNF-β, GM-CSF, and IFN – γ
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DTH Response
Type IV rxns marked by time delay and recruitment of
MØ instead of Neut’s and Eosino’s
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Cellular Interactions
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1) Mechanical Triggering of Mast Cell Degranulation (Visualize rise in intracellular Ca++)
RBL cells (rat basophilic leukemia) in culture.
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2) Spread of degranulation via soluble factor(s)...
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…i.e., release of ATP, activation via P2 receptors
Osipchuk & Cahalan, 1992
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Acute response: Mast cell mediators
Chronic response: Recruitment of cells by chemotactic
factors; production of TH cytokines, destructive
activities of eosinophils, macrophages & PMNs
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Immediate vs. late phase response in skin (above) and lung (below)
fluids eosinophils
(& PMNs..)
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Positive Tuberculin Reaction
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Contact Dermatitis
Maybe due to either TH1 or CTL mediated hypersensitivity
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Dermatitis kontak
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Hipersensitivitas tipe V
Tipe tambahan
Antibodi mengenali dan mengikat reseptor
permukaan sel
Mencegah ikatan ligan
Memperbaiki signal sel
Contoh penyakit : - Grave’s disease
- Myasthenia gravis
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