hypersensitivity international.ppt

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