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HYPERSENSITIVITY INTERNATIONAL.ppt
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HYPERSENSITIVITYRANDANAN BANDASO
DEPARTMENT OF ANATOMY PATHOLOGYFACULTY OF MEDICINE
HASANUDDIN UNIVERSITY
CAUSESOF
ILLNESOF
HUMANBEING
INFECTIONNUTRITION
NEOPLASM DEGENERATI0N
IMMUNOLOGIC
GENETICMETABOLIK
IMMULOGIC SYSTEMOF THE BODY
THE WORLD FULL OF MICROORGANISM WHICH IS DANGEROUS TO OUR BODY
SINCE BIRTH OUR BODY COMPLETED WITH THE IMMUNE SYSTEM
SOMETIMES THE SYSTEM DOES NOT WORK
IMMUNOLOGIC SYSTEM
• IMMUNITY ORGANSBONE MARROWTHYMUS
GALT =GUT ASSOCIATET LY.TIS. MALT = MUCOSA -”-BURSA FABRICUS
• IMMUNITY CELLS
IMMUNITY CELLS
• T LYMPHOCYTES
• B LYMPHOCYTES
• MACROPHAGE
• DENDRITIC AND LANGERHANS CELLS
• NATURAL KILLER CELLS
VERY USEFUL
IT CAN BE DANGEROUS
IMMUN RESPONS LIKE TWO EDGES SWORD
IMMUNITY RESPONSE
DEF.IMUN
AUTOIMUN
ECXESSREACTION
HYPERSENSITIVITY
PENIMBUNAN IG
AMYLOIDOSIS
HYPERSENSITIVITY:
1.TYPE 1 (ANAPHYLACTIC REACTION)
2.TYPE 2 (CYTOYOXIC REACTIONS)
3.TYPE 3 (IMUNOCOMPLEX)4.TYPE 4 (DELAYED
HYPERSENSITIVITY)
TYPE 1 (ANAPHYLACTIC
•SYSTEMIC•LOCAL
ATOPIC ALERGY
SYSTEMIC
• ANTIGEN ENTER THE BODY PARENTERALLY
• FOREIGN SERUM (Horse antitetanus-serum).
• DRUG (eg Penicillin)• THE BITE OF AN INSECT
SYMPTOMS OF SYSTEMIC REACTION
• REACTIONS VERY QUICK (MINUTES)
• DYSPNOE (BRONCHOSPASM, LARYNGEAL OEDEMA)
• SKIN RASHES
• DIARHEA AND VOMITING
• FALL IN BLOOD PRESSURE
• OCCASIONALLY DEATH
BEHAVIOUR OF ANAPHYLACTIC REACTIONS
• ANTIGEN:FOREIGN PROTEIN (Horse
Antitetanus Serum
DRUG (Penicillin)• DEGREE OF REACTION DEPENDS ON
LEVEL OF SENSITATION• SCHOK DOSE CAN BE VERY SMALL
• CAN CAUSES DEATH !
LOCAL ANAPHYLACTIC
• ALSO CALLED ATOPIC ALLERGY• 10% OF POPULATION• ALLERGENS:
HAUSE DUST, ANIMAL HAIR, FLOWER, FOOD: NUTS,FISH STRAWBERRIES• FAMILY HISTORY(50%)• SERUM IgE MORE THAN NORMAL
LOCAL REACTION
• SKIN CONTACT ANTIGEN URTICARIA
• GASTROINTESTINAL INGESTION DIARHEA
• LUNG INHALATION BRONCHOCONTRICTION
• NOSE INHALATION RHINITIS
• LOCAL REACTION SYSTEMIC
AL
LE
RG
EN
REACTION
ITCHINGOBSTRUCTION OF
THE NOSESECREET FROM
THE NOSESNEEZING
RHINITIS ALLERGICA
POLLEN
HOUSEDUSTMITES
ANIMALDANDER
SYSTEMIC REACTION
PARENTRAL ADMINISTRATION WITHIN MINUTES ITCHING AND URTICARIA RESPIRATORY DIFFICULTY VOMITING, ABDOMINAL CRAMPS DIARHEA SYSTEMIC VASODILATATION CIRCULATORY COLLAPSE DEATH
FIRST CONTACT :
SENSITAZATION---PRODUCTION OF IgE
MEDIATOR RELEASED
ANTIGEN
INITIAL ANDLATE PHASERESPONSES
Release of primaryAnd secondary mediator
Signal
Granules
Degranulation
Antigen
IgeSIGNALS SITOKIN
SIGNALS UTKAKTIVASI PHOSPHOLIPASE A2
PHOSPHOLIPASEA2
ACTIVE PHOSPHOLIPASEA2
MEMBRAN PHOSPHOLIPID
MEDIATOR
• PRIMARY MEDIATOR:IN THE GRANULES OF MAST
CELL
• SECONDARY MEDIATOR:LIPID MEDIATORCYTOKINES
PRIMARY MEDIATOR
• BIOGENIC AMINES:HISTAMINE: CONTRACTION OF SMOOTH MUSCLEI
OTOT POLOS, INCREASED NASAL SECRETION GASTRIC JUICE INCREASE
ADENOSINE INCREASED MEDIATOR OF MAST CELLS INHIBIT AGREGATION OF PLATELET
• CHEMOTACTIC• ENZYMES• PROTEOGLYCANS
SECONDARY MEDIATOR
• LEUKOTRIENESLEUK.C4 and D4
VASOAKTIF/SMOGENIC.LEUK.B4
STRONG CHEMOTACTICFOR EOS,NEUT DAN
MONOCYTE• PROSTAGLANDIN
PROST.D2BRONCHOSPSM+ MUCUS SECR.
SECONDARY MEDIATOR
• PAFPLATELET AGREGATION,RELEASE HIST-->BRONCHOSPA
VASODELATATION• CYTOKINES
TNFIL1,IL3,IL4,IL5.IL6
CYTOKINES INVOLVED IN TYPE 1
• IgE PRODUCTIONTH2 IL4,IL5,IL6 TH1 IFGAMMA DOWN REGULATE.
• MAST CELL GROWTHIL3,IL4
• EOS. GROWTH AND ACTIVATION . IL5 FROM TH2
ANAPHYLACTOID
• CYTOKINES (IL8)• CODEINE,MORPHINS• MELLITIN (IN BEE VENOM)• PHYSICAL STIMULI:
HEAT,COLD, SUNLIGHT• STRES ? SEING MOTHER IN LAW
ASTHMA
HYPERSENSITIVITY
TYPE II
HYPERSENSITIVITY TYPE II
• ANTIBODY TO THE ANTIGEN IN SURFACE OF THE CELLS OR COMPONENTS OF TISSUE
• ANTIGEN:INTRINSIC
EXOGEN
HIPERSENSITIVITY TYPE 2
• COMPLEMENT- DEPENDENT REACTIONS (REACTION DEPENDS ON COMPLEMENT)
• ANTIBODY- DEPENDENT CELL MEDIATED CYTOXICITY
• ANTIBODI MEDIATED CELLULAR DYSFUNCTION
COMPLEMENT DEPENDENT REACTION
ANTIBODY + ANTIGEN ---->AKTIVATION COMPONENT ---->MEMBRANE ATTACK COMPLEX
AND FIXATION ANTIBODY WITH A COMPL C3B--> OPSONIZATION.
ADCC
ANTIBODY DEPENDENT CELL MEDIATED CYTOXITY (ADCC)-->NOT NEED PHAGOCYTOSIS.LYSIS DONE BY MONOCYT, EOS, NEUT WHICH
HAVE FC RECEPTOR.
EXAMPLES OF TYPE II
• TRANSFUSION REACTION• ERYTHROBLASTOSIS FOETALIS• AHA (AUTOIMMUNE HEMOLYTIC ANAEMIA)• DRUG REACTION• MYASTHENIA GRAVIS AND GRAVE
DISEASE
A. Complement dependent
Target cell
Opsonic adherence and phagocytosis
TYPE II REACTION
MEMBRANEATTACK
COMPLEX
LYSIS
TARGET CELL
MACROPHAGE
FC RECEPTOR
ADCC=ANTIBODY DEPENDENT
CELL MEDIATED CYTOXITY
ACETHYLCHOLINE
BREAKS BYACETHYLCHOLINESTRASE
NER
VE
MUSCLE
MYASTHENIA GRAVISTHE BODY PRODUCE
ANTIBODYTO ACTH RECEPTOR
EXCESS PRODUCTION
THYROID HORMONE
THYROID CELLS
ANTIBODY TO
TSH RECEPTOR
TSHRECEPTOR
TYPE II HYPERSENSITIVITY GRAVE’S DISEASE
FATHER(DD,Dd)
MOTHER(dd)
FIRST BABY(Dd)
Rhesus+
BORN ALIVE
THE NEXT BABIESSTILL BIRTH
(Erythrocyt lysis)
ERYTHROBLASTOSIS(mother form antibody
to her baby)
HYPERSENSITIVITY
TYPE III
TYPE III REACTION
INDUCTION BY ANTIGEN-ANTIBODY COMPLEX WHICH CAUSES DEXTRUCTION OF TISSUE AS CONSEQUENCE OF ITS ABILITY TO ACTIVATE MEDIATORS EXPECIALLY COMPLEMENT.
TYPE III HYPERSENSITIVITY
• SYSTEMIC SYSTEMIC IMMUNE COMPLEX DISEASE
• LOCAL.LOCAL IMMUNE COMPLEX DISEASE (ARTHUS REACTION)
TYPE OF REACTION
• ANTIGEN : EXOGEN-ENDOGEN• LOCAL OR SYSTEMIC• THREE PHASES:
1.FORMATION AG-AB COMPLEX IN THE CIRCULATION
2.DEPOSITION AG-AB COMPLEX 3.INFLAMMATORY REACTION• DEPOSITION AG-AB COMPLEX: KIDNEY,
JOINT, SKIN, HEART, BLOOD VESSEL.
TYPE III REACTION
B CELL
ENDOTHEL.
PLASMA CELL
FREE ANTIBODY
ANTIGEN-ABCOMPLEX
PHASE 2
MAST CELL
AG-AB COMP
PHASE 3 :COMPL.MEDIATED IMFL.
COMPLMNT
PMN
LYSOSOME
DEG.FIBRINOID
PLATELETAGREGATE
IMMUNE COMPLEX VASCULITIS
HYPERSENSITIVITY
TYPE IV
TYPE IV HYPERSENSITIVITY (CELL MEDIATED)
• DELAYED TYPE HYPERSENSITIVITY• TRANSPLANT REJECTION• MECHANISM INVOLVED IN
REJECTION• METHODS OF INCREASING GRAFT
SURVIVAL• TRANSPLANTATION OF OTHER
SOLID ORGANS• TRANSPLANTATION OF
HEMOTOPOETIC CELLS
TYPE IV REACTION
• INDUCTION BY SENSITIZED T CELLS
• 2 TYPE:CLASIC: CD4+ TCELL
DIRECT CYTOTOXITY-->
CD8+ TCELL.
• M.TBC,VIRUSES, FUNGI, PROTOZOAAND PARASIT
CLASSICAL TYPE IV REACTION
• TUBERCULIN
• PROTEIN LIPOPOLYSACHARIDE(M.TBC).
• SENSITATION AFTER 8-12 HOURS , MAXSIMAL AFTER 24-72 HOURS.
• THE PROCES :CD4+TCELLS--> CONTACT WITH
ANTIGEN --> TH1 CELL.
TYPE 4 REACTION (DIRECT)
• CD8+TCELLS KILLS ANTIGENBEARING TARGETCELL
• CALLED CYTOTOXIC T LYMPHOCYTE (CTLs)
• CTLs PLAYS ROLES IN: GRAFT REJECTIONRESISTENCY TO VIRUS
INFECTION TUMOR IMMUNITY
CYTOKINES IN TYPE4 REACTION
• MACROPHAGE ATTACK M.TBC• MACROPHAGE PRODUCE IL12• IL12-->CD4TCELLS --TH1 CELLS.• TH1 CELLS -> IFN GAMMA -----
>ACTIVATE --> MACROPHAGE -->FIBROSIS.
• IL2--AUTOCRINE/PARACRINE• TNF ALPHA DAN LIMFOTOXIN-->
VASODELATATION, ADHESION, CHEMOTACTIC
LYMPHOCYT MACROPHAGE
PROCES IN THE FORMATION OFGRANULOMA
SCHEME OFDESTRUCTION OFGRAFT 1
2
1
2
ACUTE CELLU-LAR REJECTIONOF RENALALLOGRAFTMANIFEST BYA DIFFUSE MONONUCLEAR CELLINFILTRATE ANDINTERTITIALEDEMA
MONONUCLEAR
REJECTION REACTIONBY HUMORAL IN KIDNEY TRANSPALNTATION
•THICKNENING OF TUNICA INTIMA•INFLAMMATION
ACUTE VASCULITIS INTIMA MARKEDLY THICKENED AND INFLAMED