Kuliah Reaksi Hipersensivitas & Auto Imun

8/18/2019 Kuliah Reaksi Hipersensivitas & Auto Imun

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REAKSIH IPERSEN SIVITAS &

AU TO IM U N

dr.HOTMEN SIJABAT, SpPD


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Sistem Imun Terdiri atas sistem imun nonspesifk(natural/innate) dan sistem imunspesifk (adaptive/acquires) Komponen sistem imun nonspesifk : Fisik

(kulit,selaput lendir), larut (lisozim, asamlambung) selular (M, !M, k)

Komponen sistem imun spesifk :"umoral, seluler


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Sistem im un spesifik

Kemampuan untuk mengenalbenda (antigen) #ang dianggap

asing bagi dirin#a "an#a dapat men#ingkirkan

benda asing #ang suda$

dikenal sebelumn#a %istem imun spesifk $umoral

%istem imun spesifk selular


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&im'osit sal dari Multipoten, sumsum tulang *i'erensiasi dalam sumsum tulang

enda asing akan merangsang sel akanberdi'erensiasi dan proli'erasimembentuk antibodi Membentuk antibodi dilepas ke dalam serum

Fungsi antibodi perta$anan ter$adap in'eksiekstraselular, virus , bakteri dan menetralisirtoksin

Memori ter$adap perta$anan #angdi$asilkan berta$an lama


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Antibodi

Antibodi =immunoglobulins (+g)

+naktivasi antigen

dengan cara Fiksasi komplemen etralisasi glutinasi !resipitasi

amma globulin : +g-.0, +g-120, +gM-30,+g*-10, and +g4-565570

+g dapat mela8atisa8ar dara$ plasenta


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Reaksi hipersensivitas

Klasifkasi menurut ell dan9oomb

Tipe + eaksi $ipersensivitas cepat +g4, T$7, selmast, eosinofl

Tipe 76 antibodi ter$adap sel +gM, +g ter$adap permukaan sel atau antigen

matriks ekstraselular

Tipe ;6 Kompleks antibodi dan antigen

Kompl imun #ang terdiri atas antigen dalamsirkulasi dan +gM atau +g; #ang diendapkandalam membran basal vaskuler

Tipe


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Reaksi tipe I

= anaflaksis atau reaksi alergintigen #g masuk ditangkap 'agosit>T$7>sitokin>sel >+g46+g4 diikat ole$ reseptor +g* #g dimilikisel basofl, mast, eosinofl

+la antigen #g sama mema?an,

antigen diikat +g4 pada permukaan selmast #g menimbulkan degranulasi selmast dan mengeluarkan mediator$istamin, prostagalandin, leukotrin

sma bronkial, urtikaria, *


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+nduction and e@ector mec$anisms in t#pe 1 $#persensitivi


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Hipersensivitas tipe 2

eaksi $ipersensivitas sitotoksik *apat mengenai berbagai ?aringan dan

organ

ntigen biasan#a endogen, $apten(eksogen) dapat menempel pada membransel $ipersensitivitas tipe 7

eaksi dapat berlangsung dalam $itungan

menit sampai ?am Mediator reaksi adala$ +gM atau +g akan

mengakti'kan reseptor FcA-,

%el K akan berperan sebagai e'ektor dan

menimbulkan kerusakan melalui ntibod#


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Skem a reaksi tipe II


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Tpe II !persensiti"it. T#pe ++ responses are mediated b# immunoglobulin (+g)directed against cell sur'ace or matri= antigens, 8$ic$ initiates e@ector responses t$roug$ t$eFc receptor 'or +g (FcA) and complement6 T$e relative contributions o' t$ese pat$8a#s var#8it$ t$e +g subclass and t$e nature o' t$e antigen6 Bnl# FcA-mediated p$agoc#tosis b#macrop$ages (MC) is depicted in t$is 'igure6 ctivation o' complement components 8ould

result in binding o' 9;b to t$e red blood cell membrane, rendering red blood cells susceptibleto p$agoc#tosis and leading to 'ormation o' t$e membrane attack comple= and cell l#sis


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Mekanisme Reaksi HS Tipe III:

antigen masuk ke dalam dara$ (kapiler)

terbentukkompleks antigen dan antibodi dengan rasio 2 antigenterikat dengan 1 IgG atau IgA (monomeric yang soluble) menempel di endotel kapiler (terutama di gin?al dan

paru atau terba8a ke daera$-daera$ dengan aliran

dara$ #ang turbulen)

men#ebabkan inDamasi mengakti'kan sistem komplemen mengakti'kan9;a, 9


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PEN YAKIT KO M PLEKS IM U N :Sebab, Antigen dan Tem patM engendap

Sebab Antigen Tempat

KompleksMengendap

Infeksi persisten Antigen Mikroba Organ yangdiinfeksi, ginjal

Auto imunitas Antigen sendiri Ginjal, sendi,

pembuluh darah,

kulit

Ekstrinsik Antigen lingkungan Paru


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TYPE III HYPERSENSITIVITY

Penicillin

Sulfonamid


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Mekanisme Reaksi HS Tipe IV :

+munopatologi diperantarai ole$ T cell danmelibatkan dela# $#persensitivit#

gE !9(sel &anger$ans, kup'er, dendritik)> dikenali sel lim'osit (butu$ memori T cell

spesifk t$d g ) > sensitisasi sel >melepaskan mediator inDamasi


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TYPE IV HYPERSENSITIVITY


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Tpe I# !persensiti"it. T#pe + responses are mediated b# T cells t$roug$ t$ree di@erentpat$8a#s6 +n t$e frst, t#pe 1 $elper T (T"1) cells recognize soluble antigens and releaseinter'eron-A (+F-A) to activate e''ector cells, in t$is case macrop$ages (MG), and cause tissuein?ur#6 +n T"7-mediated responses, eosinop$ils predominate6 T"7 cells produce c#tokines to

recruit and activate eosinop$ils, leading to t$eir degranulation and tissue in?ur# l#mp$oc#tes(9T&s)6 +n t$e t$ird pat$8a#, damage is caused directl# b# c#tol#tic T6 +&, interleukin


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Autim m une di!"de"!

n autoimmune disorder isa condition t$at occurs

8$en t$e immune s#stemmistakenl# attacks anddestro#s $ealt$# bod#

tissue6 T$ere are more t$an 35

di@erent t#pes o'

autoimmune disorders6


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+n patients 8it$ an autoimmune

disorder, t$e immune s#stemcanHt tell t$e di@erence bet8een$ealt$# bod# tissue and antigens

T$e result is an immune responset$at destro#s normal bod# tissues6

T$is response is a$#persensitivit# reaction similar tot$e response in allergic conditions6

http://www.nlm.nih.gov/medlineplus/ency/article/000821.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000812.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000812.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000821.htm


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J$at causes t$e immunes#stem to no longer tell t$e

di@erence bet8een $ealt$#bod# tissues and antigens isunkno8n

n autoimmune disorder ma#result in: T$e destruction o' one or more

t#pes o' bod# tissue

bnormal gro8t$ o' an organ

9$anges in organ 'unction


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n autoimmune disorder ma# a@ectone or more organ or tissue t#pes6

Brgans and tissues commonl# a@ectedb# autoimmune disorders include:

lood vessels

9onnective tissues 4ndocrine glands suc$ as t$e

t$#roid or pancreas

oints Muscles

ed blood cells

%kin

http://www.nlm.nih.gov/medlineplus/ency/article/002351.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/002351.htm


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person ma# $ave more t$an one autoimmunedisorder at t$e same time6 4=amples o' autoimmune(or autoimmune-related) disorders include:

ddisonHs disease

9eliac disease - sprue (gluten-sensitive enteropat$#)

*ermatom#ositis

raves disease

"as$imotoHs t$#roiditis

Multiple sclerosis

M#ast$enia gravis

!ernicious anemia

eactive art$ritis

$eumatoid art$ritis %?ogren s#ndrome

%#stemic lupus er#t$ematosus

T#pe + diabetes

http://www.nlm.nih.gov/medlineplus/ency/article/000378.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000233.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000233.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000839.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000358.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000371.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000737.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000712.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000569.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000440.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000431.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000456.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000435.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000305.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000305.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000435.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000435.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000456.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000456.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000431.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000440.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000569.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000712.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000737.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000371.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000371.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000358.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000839.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000233.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000233.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/000378.htm


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%#mptoms o' an autoimmune

disease var# based on t$e diseaseand location o' t$e abnormalimmune response6

%#mptoms t$at o'ten occur8it$ autoimmune diseasesinclude:

Fatigue Fever

eneral ill-'eeling (malaise)

http://www.nlm.nih.gov/medlineplus/ency/article/003088.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003089.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003089.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003088.htm


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%igns depend on t$e t#pe o'disease6

Tests t$at ma# be done todiagnose an autoimmune disorderma# include: ntinuclear antibod# tests

utoantibod# tests

99

9-reactive protein (9!)

4r#t$roc#te sedimentation rate (4%)

http://www.nlm.nih.gov/medlineplus/ency/article/003642.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003356.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003638.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003638.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003356.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/003642.htm


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T$e goals o' treatment are to:

educe s#mptoms 9ontrol t$e autoimmune process

Maintain t$e bod#Hs abilit# to

fg$t disease

J$ic$ treatments are used

depends on t$e specifcdisease and #our s#mptoms6


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Medicines are o'ten prescribedto control or reduce t$eimmune s#stemHs response6

T$e# are o'ten calledimmunosuppressivemedicines6

%uc$ medicines ma# include

corticosteroids (suc$ asprednisone) and nonsteroiddrugs suc$ as azat$ioprine,

c#clop$osp$amide

Kuliah Reaksi Hipersensivitas & Auto Imun

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