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1 REAKSI HIPERSENSITIVITAS Febtarini, R, dr. Sp.PK Bagian Patologi Klinik FKU - UWKS Jum’at, 10-Januari-2014.

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Presentasi berjudul: "1 REAKSI HIPERSENSITIVITAS Febtarini, R, dr. Sp.PK Bagian Patologi Klinik FKU - UWKS Jum’at, 10-Januari-2014."— Transcript presentasi:

1 1 REAKSI HIPERSENSITIVITAS Febtarini, R, dr. Sp.PK Bagian Patologi Klinik FKU - UWKS Jum’at, 10-Januari-2014

2 ANATOMY OF THE IMMUNE SYSTEM

3 CELLS OF THE IMMUNE SYSTEM

4 Schematic diagram of structure of Ig Glycoprotein Polypeptide : 82-96% Cbh : 2-14%

5 ANTIBODIES STRUCTURECLASS

6

7 Ag can bind in pockets or grooves or on extended surfaces in the binding sites of Abs

8 8 VON PIRQUET (1906) –Aktivitas berubah –Reaktivitas berubah –Energi berubah atau : Reaksi abnormal oleh adanya suatu rangsangan COCA DAM COOKE (1923) Atopi : reaksi alergi yang dipengaruhi oleh faktor keturunan (herediter) SENSITISASI: Membuat (sesorang) menjadi reaktif terhadap zat asing HIPERSENSITIVITAS : Reaksi alergi REAKSI IMUNOLOGIS –Antigen – Antibody (Zat Anti) –Limfosit Sensitif

9 9 ANTIGEN Zat asing yang dapat merangsang pembentukan antibody Antigen= Alergen = Imunogen = Atopen SYARAT ANTIGEN –Umumnya protein asing –Berat molekul besar –Bentuk tetap –Mampu menginduksi pembentukan AB –Dapat dihancurkan oleh sel-sel tubuh –Penting jumlah optimal untuk dapat merangsang pembentukan AB cukup tinggi

10 10 HAPTEN –Zat Kimia –Berat Molekul (rendah) kecil –Bila bergabung dengan protein badan  Antigen HP A

11 11 REAKSI HIPERSENSITIFITAS Menurut Gell & Coombs  4 type Type I= Reaksi Cepat = Reaksi Anafilaksis = Reaksi Reagin Dependent = Immediate Hypersensitivity R Type II= Reaksi Sito-toksik Type III= Reaksi Antigen-Antibody kompleks Type IV= “Cell Mediated Immun Reaction”

12 Gell And Coombs Classification Of Immune-mediated Allergic Response TYPEMECHANISMMANIFESTATIONS IIgE –dependent Anaphylaxis, urticaria II Complement-mediated cytotoxicity Cytopenias III Immune complex deposition Vasculitis / nephritis IV Delayed-type hypersensitivity Dermatitis or hepatitis

13 13 REAKSI TYPE I DASARNYA: Ig E melekat pada dinding sel mast Antigen terikat Fab dari Ig E Terjadi degranulasi sel mast Pengeluaran vasoaktif amin Timbul gejala klinik : Vasodilatasi, Permeabilitas, Perdarahan , exudasi, edema, obstruksi bronkus, kontraksi otot polos.

14 14 CONTOH REAKSI TYPE I : –Asma Bronkial Ekstrinsik –Rinitis Alergika –“Hay Fever” (Demam Rumput) –Beberapa Jenis Urtikaria –Angioneurotik Oedema –Alergi Obat –Alergi Makanan –Gigitan Serangga –Anafilaksis Sistemik –Dermatitis Atopik –Eksim

15 Allergy (type I hypersensitivity mediated by IgE on mast cells)

16 16 CARA ANTIGEN MASUK BADAN –Kontak langsung dengan permukaan kulit –Jalan nafas ( A. Inhalan) –Traktus Digestivus –Parenteral MACAM ALERGEN: –Inhalan: Debu Rumah, Tungau, Jamur, Tepung Sari, Rumput, Serpih Kulit –Ingestan: Susu, telur, ikan, kacang-kacangan (Makanan) –Injectan:  obat-obatan Penisilin, Streptomisin (Parenteral) –Lain-lain: Virus/produk bakteri –Contactan: Obat-obatan, Zat-zat Kimia

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18 18 REAKSI TYPE II DASAR: Yang berperan: IgG, IgM Antigen pada dinding sel, dapat berupa Hapten Antibody spesifik terikat pada antigen Kadang-kadang mengikat Complement Sel Lisis

19 19 Antibody Complement Cytolysis Antibody Red blood cell Antigen

20 20 CONTOH REAKSI TYPE II : –Alergi Obat/Zat Kimia Lain –Anemia Hemolitik –Purpura –Trombositopenia, Pansitopenia karena Alergi obat/Zat kimia lain –Beberapa Penyakit Autoimun –Miastenia gravis –Thyroiditis Chronis –Acut Post Streptococcus G. Nephritis

21 Reaksi hipersensitifitas tipe 3 Reaksi kompleks imun (Ag-Ab) di jaringan atau pembuluh darah Ig G Kompleks imun  mengaktifkan komplemen  kemotaktik faktor  makrofag ke jaringan  merusak jaringan 21

22 22 Ag-Ab Complex Platelet Aggregation Complement activation Microthrombi Vasoactive amine release Attract Polymorphs Anaphylatoxin Release proteolytic enzymes and polycationic proteins from granules Histamin release Figure 6.3 Type III Complex-mediated hypersensitivity

23 23 CONTOH KHAS R. TYPE III –Arthus Phenomen –Serum Sickness –Penyakit Autoimun CONTOH DALAM KLINIK: –Rheumatoid Arthritis –Serum Sickness Syndrome –Alergi Obat –Peri Arteritis Nodosa –Sub Acut / Chronic G.N –Extrinsik Alergik Alveolitis

24 24 REAKSI TYPE IV SKEMA: Ikatan antara Ag oleh T Limfosit Pelepasan Mediator dgn Aktivitas Biologis yang luas (MAF) Akibatnya memperbesar Imun respons selluler Akumulasi sel Macrophag & Leukocyt ke tempat reaksi Nekrose Jaringan, Ulserasi lokal

25 25 DASAR R. TYPE IV –Reaksi terjadi antara Ag. Spesifik dengan limfosit sensitif –Pelepasan Lymphokins –Menimbulkan sitotoksik langsung tanpa melibatkan lg & complement CONTOH: –Sensitivitas reaksi thd TBC –Reaksi thd Transplantasi –Tumor Imunitas –Contact Dermatitis

26 26 KARAKTERISTIK REAKSI HIPERSENSITIFITAS –Sering akut –Kronis –Rekuren (Kumat-kumatan) –Organ sasaran berubah Satu (single) alergen  bermacam-macam manifestasi klinik Satu (single) manifestasi klinik : dapat disebarkan oleh banyak alergen A ASMA RINITIS DERMATITIS SYOK ANAFILAKSIS D.L.L ASMA MACAM-MACAM ALERGEN A. INHALAN MAKANAN OBAT-OBATAN DLL

27 27 KARAKTERISTIK LAIN –Herediter (menurun) –Dapat diditeksi faktor-faktor pencetus –Intensitas: alergen dipengaruhi oleh faktor non alergen –Menunjukkan sifat hiperreaktif DIAGNOSIS (ATAS DASAR): –ANAMNESIS:- Riwayat Penyakit- Faktor Pencetus - Gejala (keluhan)- Faktor Keluarga - Perjalanan Penyakit –FISIK:Tergantung organ sasaran “Wheezing” Mukosa Hidung oedem Urtika, syok, dll

28 28 MACAM-MACAM TES: –Tes Kulit –Tes Provokasi Bronkial –Tes Latihan(Exercise) LABORATORIUM PENTING –Jumlah Eosinofil –Kadar Ig E (Total/spesifik) dalam PEMERIKSAN LAIN X Foto:Thorax Sinus Paranasalis

29 29 MEDIATOR2 PENTING DALAM REAKSI HIPERSENSITIFITAS HISTAMIN:- Dalam sel mast- Kontraksi otot polos - Dilatasi pembuluh darah- Permeabilitas ↑↑ - Exudasi- Oedema LEUKOTRINE :- SRS-A (SlowReactinSubtance of Anaphylaxis) - Kontraksi otot polos SEROTONIN:- Dilatasi pemb. Darah- Permeabilitas ↑↑ - Bronkus Obstruksi Diagnosis: ►Anamnesis►Lab: Ig.E, Eosinofil ►Fisis►Faal Nafas ►X-Foto►Tes Kulit ►Tes Provokasi

30 30 SHOCK ORGAN (ORGAN SASARAN) Digunakan oleh DOERR (1922) Artinya: Organ atau jaringan tempat timbulnya reaksi alergi Misalnya: Penyakit Organ Sasaran ASMA …………………………Jl. Nafas URTIKA ………………………Kulit RINITIS ………………………Hidung MIGRAIN …………………….S.S.P DIARE ………………………..Tract Digest CONJUNCTIVITIS ………….Mucosa Mata NEUROMIALGIA ……………Sistem Neuro Musk

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32 32 CYTOKINE ADHESION MOLECULES Bagian Patologi Klinik FKU-UWKS

33 33 ANTIGEN -Bakteri -Virus -Parasit -Zat-zat asing -Dll TERPAPAR (PAPARAN) (EXOGEN) FISIK TERMIS MEKANIS RADIASI PSIKIS STATUS NUTRISI R.I.S  R.I.H KELEMAHAN UMUM INAKTIVITAS DLL ALERGEN IMUNOGEN R.I. ABNORMAL (MENYIMPANG) PROTEKSI SUB NORMAL S.I DEF RADIASI OBAT-OBATAN ZAT-ZAT TOKSIS DLL IMUN (KEBAL) KLINIK ALERGI A.I. GEN R.I 01

34 34 FUNGSI CYTOKINE MENGATUR (REGULATE) –PERTUMBUHAN SEL –MEMACU AKTIFITAS SEL –PROSES INFLAMASI –PROSES IMUNITAS –TISSUE REPAIR –PROSES FIBROSIS –MORFOGENESIS 02

35 35 IL4IL5 NK cells T cells Costimulant of T cells proliferation Costimulant of B cells proliferation Bone marrow precursor cell proliferation Macrophage activation and differentiation Mast cell proliferation Eosinofil proliferation IL-4 + Ig E + MHC class II + FcR epsilon + IgA myelopoiesis + MHC class II Figure 7-4. Cell sources and target cell effects of IL-4 and IL-5 Target cell effects Cell sources IL-5 03

36 36 Transforming Growth Factor (TGF-β) Figure 7-4. Cell sources and target cell effects of TGF-β Inhibits T cell proliferation and lymphokine production Inhibits B cell proliferation and antibody production Inhibits early hematopoietic stem cell replication Attract macrophages Inhibits natural killer activity Osteoclast activation in bone Stimulates and mobilizes fibroblasts  wound healing + collagen, fibronectin and collagenase Suppresses proliferation of epithelial cells, fetal hepatocytes, and endothelial cells T cells B cells macrophages Platelets Placenta, bone and kidneys Cell sources Target cell effects 04

37 37 TNF-α and TNF-β (LT) Macrophages  prostaglandins and mediates cytocidal activation  IL-1, IL-6,IL-8. GMCSF Bone Marrow Inhibits in vitro hematopoiesis but stimulates CSF in vivo PMN’s Neutrophilia Metabolic activation chemoattracts B-Lymphocytes Proliferate  antibody production  lymphokine production  IL-2 receptors IFN CSF IL-4 LDCF IL-2 T-Lymphocytes IL-2, IL-4 IFN-γ 05

38 38 IL-1 α and β Macrophages  prostaglandins and cytocidal activation  IL-6,  IL-8,  GMCSF,  TNF,  PA,  I-CAM 1 Bone Marrow hematopoiesis but  CSF PMN’s Neutrophilia Metabolic activation B-Lymphocytes Proliferate  antibody production  lymphokine production IFN CSF IL-4, IL-5 LDCF IL-2 T-Lymphocytes IL-2, IL-4 IFN-γ 06

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41 41 Table 7-1. Characterictic properties of cytokines CytokineMWPrincipal Cell SourcesPrimary Type of ActivityPreeminent Effects IL-1 17,500Macrophahes and others (see Table 7-2) ImmunoaugmentationInflammatory and hematopoietic IL-2 15,500T Lymphocytes and LGLT and B Cell growth factorActivates T and NK cells IL-3 14,000-28,000T LymphocytesHematopoetic growth factorPromotes growth of early myeloid progenitor cells IL-4 20,000T H CellsT and B cell growth factor; promotes IgE reactions Promotes Ig E switch and mast cell growth IL-5 18,000T H CellsStimulates B cells and eosinophilsPromotes IgA switch and eosinophilia IL-6 22,000-30,000Fibroblast and othersHybridoma growth factor; augments inflammation Growth factor for B cell and polyclonal immunoglobulin production IL-7 25,000Stromat cellsLymphopoietinGenerates pre-B and Pre-T cells and is lymphocyte growth factor IL-8 8,800Macrophages and othersChemoattracts neutrophils and T Lymphocytes Regulates lymphocyte homing and neutrophil infiltration G-CSF 18,000-22,000Monocytes and othersMyeloid Growth factorGenerates neutrophil M-CSF 18,000-26,000Monocytes and othersMacrophages growth factorGenerates macrophage GM-CSF 14,000-38,000T cells and othersMonomyelotic growth factorMyelopoiesis IFN α 18,000-20,000LeukocytesAntiviral, antiproliferativee, and immunomodulating Stimulates macrophages and NK cells Induce cell membran antigens (eg, MHC) IFN β 25,000Fibroblasts IFN γ 20,000-25,000T-Lymphocytes and NK cells TNF α 17,000Macrophages and othersInflammatory, immunoenhancing, and tumorcidal Vascular thromboses and tumor necrosis LT=TNFβ 18,000T-Lymphocytes TGF-β 25,000Platelets, bone and othersFibroplasia and immunosuppressionWound healing and bone remodelling 09

42 42 The main feature of the best-studied cytokines CytokineMol.wtCell source(s)Main cell target(s)Main actions IFN γ (dimer)T cells, NK cellsLymphocytes, monocytes, tissue cells Immunoregulation, B cell differentation, some antiviral action IL-1 α IL-1β Monocytes, dendritic cells, some B cells, fibroblasts, epithelial cells, endothelium, asctrocytes, macrophages Thymocytes, neutrophils, T and B cells, tissue cells Immunoregulation, inflammatory, fever IL T cellsT cells, B cells, monocytes Proliferation, activation IL T cellsStem cells, progenitorsPan-specific colony stimulating factor IL T cellsB cells, TcellsDivision and differentiation IL-5? (153 aminoacids) T cellsB cells, eosinophilsDifferentiation IL Macrophages, T cell, fibroblasts, some B cells T cells, B cells, thymocyets, hepatocytes Differentiation, acute phase protein synthesis IL-8 (Family) 8.000Macrophages, skin cellsGranulocyte, T cellsChemotaxis TNF α Macrophages. lymphocytes Fibroblasts, endothelium Inflammation, catabolism (cachexia), fibrosis, production of other cytokines (IL-1, IL-6, GM-CSF) and adhesion molecules TNFβ (Lymphotoxin) Fig Summary of the main features of the best studied from study of cDNA sequences. Only the most important cytokines. In some cases the molecular weight is derived targets and action are shown 10

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