Hypersensitivity refers to undesirable reactions produced by the normal immune system. The document discusses the different types of hypersensitivity reactions including: Type I reactions are rapid allergic reactions mediated by IgE antibodies and mast cells. Type II reactions involve cytotoxic antibodies attacking cell surfaces and can cause conditions like hemolytic disease of the newborn. Type III reactions involve immune complex deposition leading to conditions like serum sickness. The document provides detailed explanations and examples of each hypersensitivity type.

1. Disorders of Immunity – 3Disorders of Immunity – 3
HypersensitivityHypersensitivity
Dr.CSBR.Prasad, M.D.Dr.CSBR.Prasad, M.D.
APR-2015-CSBRP

2. Disorders of Immune system
 Hypersensitivity reactionsHypersensitivity reactions
 Autoimmune diseasesAutoimmune diseases
 Immunologic deficiency syndrome – AIDSImmunologic deficiency syndrome – AIDS
 AmyloidosisAmyloidosis
APR-2015-CSBRP

3. Disorders of Immune system
Hypersensitivity reactionsHypersensitivity reactions
Definition:Definition:
The termsThe terms HypersensitivityHypersensitivity oror AllergicAllergic statestate
refer to anrefer to an altered immune statealtered immune state followingfollowing
exposure to an antigen, wherebyexposure to an antigen, whereby subsequentsubsequent
contact results in tissue injurycontact results in tissue injury oror a diseasea disease..
Hypersensitivity refers to undesirable (damaging and
sometimes fatal) reactions produced by the normal
immune system
Hypersensitivity refers to undesirable (damaging and
sometimes fatal) reactions produced by the normal
immune system
APR-2015-CSBRP

4. Disorders of Immune system
Hypersensitivity reactionsHypersensitivity reactions
Protective Damaging
APR-2015-CSBRP

5. Hypersensitivity reactionsHypersensitivity reactions
 Exogenous antigensExogenous antigens
 Dust, pollen, food, drugs, microbiologicalDust, pollen, food, drugs, microbiological
agents, chemicals and blood productsagents, chemicals and blood products
 Endogenous antigensEndogenous antigens
 Blood transfusion, graft rejection, autoimmuneBlood transfusion, graft rejection, autoimmune
reactionreaction
APR-2015-CSBRP

6. Hypersensitivity reactionsHypersensitivity reactions
ClassificationClassification ((Gell & CoombsGell & Coombs))
 Type-IType-I Immediate orImmediate or AnaphylacticAnaphylactic typetype
 Type-IIType-II Cytotoxic typeCytotoxic type
 Type-IIIType-III Immune complex mediated typeImmune complex mediated type
 Type-IVType-IV Delayed hypersensitivity typeDelayed hypersensitivity type
 Type-VType-V Anti-receptor typeAnti-receptor type
 Type-VIType-VI MiscellaneousMiscellaneous
APR-2015-CSBRP

7. Hypersensitivity reactionsHypersensitivity reactions
 Type I disease ( Anaphylactic type)Type I disease ( Anaphylactic type)
 AnaphylaxisAnaphylaxis
 Bronchial asthmaBronchial asthma
 Infantile eczemaInfantile eczema
 Immediate drug reactionImmediate drug reaction
 Shock from rupture of hydatid cystShock from rupture of hydatid cyst
 Insect bite reactionsInsect bite reactions
Formation ofFormation of IgE AbIgE Ab – release of vasoactive amines &– release of vasoactive amines &
spasmogenic substances fromspasmogenic substances from basophilsbasophils andand mast cellsmast cells
followed by recruitment by other inflammatory cellsfollowed by recruitment by other inflammatory cells
APR-2015-CSBRP

8. Hypersensitivity reactionsHypersensitivity reactions
 Type II disease (cytotoxic type)Type II disease (cytotoxic type)
 Hemolytic transfusion reactionsHemolytic transfusion reactions
 HDNHDN
 Autoimmune Hemolytic anemiaAutoimmune Hemolytic anemia
 Goodpasture’s syndromeGoodpasture’s syndrome
Binding of IgG, IgM to Ag on target cell andBinding of IgG, IgM to Ag on target cell and
phagocytosis or lysis of target cellphagocytosis or lysis of target cell
APR-2015-CSBRP

9. Hypersensitivity reactionsHypersensitivity reactions
 Type III disorder (Immune complex disease)Type III disorder (Immune complex disease)
 SLESLE
 Acute glomerulonephritisAcute glomerulonephritis
 RARA
 PANPAN
 Erythema nodosumErythema nodosum
Ag-Ab complex – activate complement – attractAg-Ab complex – activate complement – attract
neutrophils – release of lysosomal enzymes andneutrophils – release of lysosomal enzymes and
toxic free radicalstoxic free radicals
APR-2015-CSBRP

10. Hypersensitivity reactionsHypersensitivity reactions
 Type IV disorder (Cell mediated/delayedType IV disorder (Cell mediated/delayed
hypersensitivity)hypersensitivity)
 Caseous necrosis in TuberculosisCaseous necrosis in Tuberculosis
 Leprosy neuritisLeprosy neuritis
 Contact dermatitisContact dermatitis
Sensitized T lymphocytes – cell mediatedSensitized T lymphocytes – cell mediated
cytotoxicitycytotoxicity
APR-2015-CSBRP

11. Hypersensitivity reactionsHypersensitivity reactions
 Type V disorder (Type V disorder (Anti-receptor typeAnti-receptor type))
 Grave’s diseaseGrave’s disease
 Myasthenia gravisMyasthenia gravis
 Insulin resistant diabetesInsulin resistant diabetes
Formed antibodies bind with receptors.Formed antibodies bind with receptors.
Results can be excessiveResults can be excessive activationactivation oror blockadeblockade
APR-2015-CSBRP

12. Hypersensitivity reactionsHypersensitivity reactions
 Type VI disorder (Miscellaneous)Type VI disorder (Miscellaneous)
They are due to pure activation of alternateThey are due to pure activation of alternate
pathway of compelmentpathway of compelment
 Gram negative endotoxic shockGram negative endotoxic shock
 PNHPNH
APR-2015-CSBRP

13. Type I HypersensitivityType I Hypersensitivity
( Anaphylactic type)( Anaphylactic type)
 Rapidly developing immunological reactionRapidly developing immunological reaction
 Systemic reactionSystemic reaction – IV injection of antigen– IV injection of antigen
 Local reactionLocal reaction – Skin / GIT / Respiratory /– Skin / GIT / Respiratory /
ConjunctivalConjunctival
APR-2015-CSBRP

14. Type I HypersensitivityType I Hypersensitivity
( Anaphylactic type)( Anaphylactic type)
 Reaction occurs inReaction occurs in 2 phases2 phases
 Intial responseIntial response – occurs within 5-30 min after– occurs within 5-30 min after
exposure to allergen & last for 60 min.exposure to allergen & last for 60 min.
Vasodilatation, vascular leakage, smooth muscleVasodilatation, vascular leakage, smooth muscle
spasm/ glandular secretionspasm/ glandular secretion
 Late phase responseLate phase response - Occurs after 2 – 8 hours- Occurs after 2 – 8 hours
without additional exposure to Ag and last forwithout additional exposure to Ag and last for
daysdays
Infiltration by eosinophils, neutrophils,Infiltration by eosinophils, neutrophils,
basophils, monocytes and CD4 T cellbasophils, monocytes and CD4 T cell
APR-2015-CSBRP

15. Mast cellsMast cells
Near blood vessels, nerves and in subepithelialNear blood vessels, nerves and in subepithelial
sitessites
 Membrane bound granules containingMembrane bound granules containing
biologically active mediatorsbiologically active mediators
 Metachromatic granulesMetachromatic granules
 Activation by cross linking of IgE FcActivation by cross linking of IgE Fc
receptor, C5a, C3a, cytokines (IL- 8), drugsreceptor, C5a, C3a, cytokines (IL- 8), drugs
(codeine, morphine)(codeine, morphine)
APR-2015-CSBRP

16. APR-2015-CSBRP

17. Figure 6-12 Pathogenesis
of immediate (type I)
hypersensitivity reaction.
The late-phase reaction is
dominated by leukocyte
infiltration and tissue injury.
TH2, T-helper type 2 CD4
cells.
APR-2015-CSBRP

18. Figure 15-10 A simplified scheme of the system of type 1 helper T (TH1) and
type 2 helper (TH2) cells.
APR-2015-CSBRP

19. Type I HypersensitivityType I Hypersensitivity
( Anaphylactic type)( Anaphylactic type)
 Primary mediatorsPrimary mediators
 Biologenic aminesBiologenic amines::
 Histamine – bronchial SM contractor, ↑ vascularHistamine – bronchial SM contractor, ↑ vascular
permeability, ↑ secretionpermeability, ↑ secretion
 Adenosine – Bronchoconstriction, Platelet aggregationAdenosine – Bronchoconstriction, Platelet aggregation
 Chemotactic mediatorsChemotactic mediators – Eosinophils, Neutrophils– Eosinophils, Neutrophils
 EnzymesEnzymes – Proteases, Acid hydrolases– Proteases, Acid hydrolases
 ProteoglycansProteoglycans – Heparin, chondroitin sulfate– Heparin, chondroitin sulfate
Major site of action of HISTAMINE: Venules
APR-2015-CSBRP

20. Type I HypersensitivityType I Hypersensitivity
( Anaphylactic type)( Anaphylactic type)
 Secondary MediatorsSecondary Mediators
 LeukotriensLeukotriens:
 C4 & D4 – vasoactive and spasmogenicC4 & D4 – vasoactive and spasmogenic
 B4- chemotactic for PMN, EØ, MonocytesB4- chemotactic for PMN, EØ, Monocytes
 Prostoglandins D2Prostoglandins D2 – Bronchospasm,– Bronchospasm,
↑secretion↑secretion
 PAFPAF – Pl. aggregation, release of histamine– Pl. aggregation, release of histamine
 CytokinesCytokines – Recruit & activate inflammatory– Recruit & activate inflammatory
cellscells
APR-2015-CSBRP

21. Figure 6-13 Activation of
mast cells in immediate
hypersensitivity and
release of their mediators.
ECF, eosinophil
chemotactic factor; NCF,
neutrophil chemotactic
factor; PAF, platelet-
activating factor.
APR-2015-CSBRP

22. Type I HypersensitivityType I Hypersensitivity
( Anaphylactic type)( Anaphylactic type)
 Immediate reactionImmediate reaction
 HistamineHistamine
 LeukotriensLeukotriens
 Late phase reactionLate phase reaction
 PAFPAF
 TNF -αTNF -α
 CytokinesCytokines
EosinophilsEosinophils – major basic protein , EØ cationic protein,– major basic protein , EØ cationic protein,
leukotriens C4, PAFleukotriens C4, PAF
Directly activate Mast cells to release mediatorsDirectly activate Mast cells to release mediators
APR-2015-CSBRP

23. Type I HypersensitivityType I Hypersensitivity
( Anaphylactic type)( Anaphylactic type)
 Systemic AnaphylaxisSystemic Anaphylaxis
 Antisera, Hormones, Enzymes, DrugsAntisera, Hormones, Enzymes, Drugs
 Itching, erythema, respiratory distress, laryngealItching, erythema, respiratory distress, laryngeal
edema, deathedema, death
 Local AnaphylaxisLocal Anaphylaxis
 Atopic allergy –Atopic allergy – Genetically determinedGenetically determined ~10% of~10% of
the populationthe population
 predisposition to develop reaction to inhaled /predisposition to develop reaction to inhaled /
ingested allergensingested allergens
 Urticaria, angioedema, allergic rhinitis, asthmaUrticaria, angioedema, allergic rhinitis, asthma
APR-2015-CSBRP

24. APR-2015-CSBRP

25. Type II HypersensitivityType II Hypersensitivity
((Cytotoxic typeCytotoxic type))
 Mediated by Abs toMediated by Abs to cell surface Agscell surface Ags andand
components ofcomponents of extracellular matrixextracellular matrix
3 mechanisms3 mechanisms
1.1. Complement dependent reactionComplement dependent reaction
2.2. Antibody dependent cell mediatedAntibody dependent cell mediated
cytotoxicity (ADCC)cytotoxicity (ADCC)
3.3. Antibody mediated cellular dysfunctionAntibody mediated cellular dysfunction
APR-2015-CSBRP

26. Complement dependent reactionComplement dependent reaction
 Direct lysis –Direct lysis –
 Membrane Attack Complex – C5-9Membrane Attack Complex – C5-9
 OpsonizationOpsonization
 Attachment of Ab/C3b fragment to cell surfaceAttachment of Ab/C3b fragment to cell surface
APR-2015-CSBRP

27. Opsonisation & cell lysisOpsonisation & cell lysis
APR-2015-CSBRP

28. Complement mediated lysisComplement mediated lysis
APR-2015-CSBRP

29. APR-2015-CSBRP

30. APR-2015-CSBRP

31. APR-2015-CSBRP

32. Complement dependent reactionComplement dependent reaction
 Transfusion reactionsTransfusion reactions
 Erythrhroblastosis fetalisErythrhroblastosis fetalis
 Autoimmune Hemolytic anemiaAutoimmune Hemolytic anemia
 Pemphigus vulgaris – Ab againstPemphigus vulgaris – Ab against
desmosomesdesmosomes
APR-2015-CSBRP

33. Antibody dependent cell mediatedAntibody dependent cell mediated
cytotoxicity (ADCC)cytotoxicity (ADCC)
 Target cells coated with IgG Ab are killed byTarget cells coated with IgG Ab are killed by
nonsensitized cells that have Fc receptornonsensitized cells that have Fc receptor
 Cell lysis without phagocytosisCell lysis without phagocytosis
 Mediated by monocytes, neutrophils,Mediated by monocytes, neutrophils,
eosinophils & NK cellseosinophils & NK cells
 Parasite, tumor cell, graft rejectionParasite, tumor cell, graft rejection
APR-2015-CSBRP

34. ADCC – apoptosis by NK cellsADCC – apoptosis by NK cells
APR-2015-CSBRP

35. 1.1. What is the % of Rh negativity?What is the % of Rh negativity?
2.2. Which HDN is more common?Which HDN is more common?
3.3. Which HDN is more severe?Which HDN is more severe?
4.4. What is RhoGAM?What is RhoGAM?
5.5. How do you assess transplacental bleed?How do you assess transplacental bleed?
6.6. How do you assess anemia in a fetus?How do you assess anemia in a fetus?
7.7. What are the other causes for Hydrops fetalis?What are the other causes for Hydrops fetalis?
Type II HypersensitivityType II Hypersensitivity
((Cytotoxic typeCytotoxic type))
APR-2015-CSBRP

36. APR-2015-CSBRP

37. Antibody mediated cellularAntibody mediated cellular
dysfunctiondysfunction
 Myasthenia GravisMyasthenia Gravis – Ab react with– Ab react with
acetochyline receptor in the motor end plateacetochyline receptor in the motor end plate
of skeletal muscle – muscle weaknessof skeletal muscle – muscle weakness
 Graves diseaseGraves disease – Ab against TSH receptor– Ab against TSH receptor
on thyroid epithelial cells - Hyperthyroidismon thyroid epithelial cells - Hyperthyroidism
APR-2015-CSBRP

38. APR-2015-CSBRP

39. Type II HypersensitivityType II Hypersensitivity
(cytotoxic type)(cytotoxic type)
 Good pasture syndrome –Good pasture syndrome –
 Type IV collagen of BM of glomeruli and lungType IV collagen of BM of glomeruli and lung
alveolialveoli
 Bullous pemphigoidBullous pemphigoid
 Epithelial BM proteinEpithelial BM protein
 Pernicious anemiaPernicious anemia
 Intrinsic factor and gastric parietal cellIntrinsic factor and gastric parietal cell
 Acute rheumatic feverAcute rheumatic fever
 Ab against streptococus cross react with heartAb against streptococus cross react with heart
APR-2015-CSBRP

40. Goodpasture
Syndrome
APR-2015-CSBRP

41. APR-2015-CSBRP

42. Bullous pemphigoidBullous pemphigoid
APR-2015-CSBRP

43. Type III HypersensitivityType III Hypersensitivity
((Immune Complex MediatedImmune Complex Mediated))
 Antigen – Antibody complexes producesAntigen – Antibody complexes produces
tissue damage by eliciting inflammation attissue damage by eliciting inflammation at
the site of depositionthe site of deposition
 Circulating immune complexesCirculating immune complexes
 Deposited in vessel wallDeposited in vessel wall
 In Situ immune complexesIn Situ immune complexes
 Extrasvascular placesExtrasvascular places
APR-2015-CSBRP

44. Type III HypersensitivityType III Hypersensitivity
(Immune Complex Mediated)(Immune Complex Mediated)
Two types of AntigenTwo types of Antigen
 Exogenous AgExogenous Ag
 Foreign protein, bacteria, virusForeign protein, bacteria, virus
 Endogenous AgEndogenous Ag
 Circulating Ag in bloodCirculating Ag in blood
 Nuclear AgNuclear Ag
APR-2015-CSBRP

45. Systemic immune complexSystemic immune complex
diseasedisease
 Acute serum sickness – injection of horseAcute serum sickness – injection of horse
serumserum
 3 phase3 phase
 Immune complex formationImmune complex formation
 Immune complex depositionImmune complex deposition
 Immune complex mediated inflammationImmune complex mediated inflammation
APR-2015-CSBRP

46. Type III HypersensitivityType III Hypersensitivity
(Immune Complex Mediated)(Immune Complex Mediated)
 Factors affecting out come of immuneFactors affecting out come of immune
complexcomplex
 Size of immune complexSize of immune complex
 Functional status of phagocyte systemFunctional status of phagocyte system
 Charge of immune complex, affinity of Ag toCharge of immune complex, affinity of Ag to
various tissue component and hemodynamicvarious tissue component and hemodynamic
factor influences tissue deposition offactor influences tissue deposition of
immune compleximmune complex
 Glomeruli, joints, skin, heart, blood vesselGlomeruli, joints, skin, heart, blood vessel
APR-2015-CSBRP

47. Type III HypersensitivityType III Hypersensitivity
(Immune Complex Mediated)(Immune Complex Mediated)
 Immune complex deposited in tissue elicitImmune complex deposited in tissue elicit
acute inflammatory reactionacute inflammatory reaction
 Fever,Fever, urticariaurticaria,, arthralgiaarthralgia, lymph node, lymph node
enlargement andenlargement and proteinuriaproteinuria
 Activation of complement cascadeActivation of complement cascade ––
 C3a, C5aC3a, C5a
 Activation of neutrophil & macrophagesActivation of neutrophil & macrophages
through their Fc receptorthrough their Fc receptor
APR-2015-CSBRP

48. APR-2015-CSBRP

49. APR-2015-CSBRP

50. Type III HypersensitivityType III Hypersensitivity
(Immune Complex Mediated)(Immune Complex Mediated)
 Release of proinflammatory mediatorsRelease of proinflammatory mediators
 PG, vasodilator peptides, chemotacticPG, vasodilator peptides, chemotactic
substances, lysosomal enzymes and oxygen freesubstances, lysosomal enzymes and oxygen free
radicals – tissue damageradicals – tissue damage
 Immune complex – platelet aggregation &Immune complex – platelet aggregation &
Hageman factor activation – microthrombiHageman factor activation – microthrombi
formationformation
 Vasulitis / GlomerulonephritisVasulitis / Glomerulonephritis
APR-2015-CSBRP

51. Systemic immune complexSystemic immune complex
diseasedisease
MorphologyMorphology
 Acute necrotizing vasculitisAcute necrotizing vasculitis
 GlomerulonephritisGlomerulonephritis ––
 SLE, Acute poststreptococcal GNSLE, Acute poststreptococcal GN
 Collagen disorderCollagen disorder
 Rheumatoid arthritis,Rheumatoid arthritis,
 polyarteritis nodosa,polyarteritis nodosa,
APR-2015-CSBRP

52. Acute necrotizing vasculitisAcute necrotizing vasculitis
APR-2015-CSBRP

53. Local immune complex diseaseLocal immune complex disease
((Arthus reactionArthus reaction))
 Localized area of tissue necrosis resultingLocalized area of tissue necrosis resulting
from acute immune complex vasculitisfrom acute immune complex vasculitis
usually in the skinusually in the skin
 Arthus lesion develop over few hours &Arthus lesion develop over few hours &
reaches peak 4-10 hours after injectionreaches peak 4-10 hours after injection
 M/S – fibrinoid necrosis of vesselM/S – fibrinoid necrosis of vessel
APR-2015-CSBRP

54. Type IV HypersensitivityType IV Hypersensitivity
(Cell mediated)(Cell mediated)
 Intiated by specifically sensitized T lymphocytesIntiated by specifically sensitized T lymphocytes
 Immunological reaction to M. Tuberculosis, virus,Immunological reaction to M. Tuberculosis, virus,
fungi, protozoa & parasitefungi, protozoa & parasite
 Contact dermatitisContact dermatitis
 Graft rejectionGraft rejection
 Two typesTwo types
1.1. Classic delayed type hypersensitivity reaction –Classic delayed type hypersensitivity reaction –
mediated by CD4 T cellmediated by CD4 T cell
2.2. Direct cell cytotoxicity - Mediated by CD8 T cellDirect cell cytotoxicity - Mediated by CD8 T cell
APR-2015-CSBRP

55. Classic delayed type hypersensitivityClassic delayed type hypersensitivity
 Tuberculin reactionTuberculin reaction
 Protein lipopolysaccharide component ofProtein lipopolysaccharide component of
tubercle bacillitubercle bacilli
 Reddening & induration of site – 8-12 hoursReddening & induration of site – 8-12 hours
 Peak in 24 – 72 hoursPeak in 24 – 72 hours
 M/SM/S
 Perivascular mononuclear cell infiltrationPerivascular mononuclear cell infiltration
 Edema & fibrin depositionEdema & fibrin deposition
APR-2015-CSBRP

56. Tuberculin testTuberculin test
APR-2015-CSBRP

57. Classic delayed type hypersensitivityClassic delayed type hypersensitivity
 Persistent / nondegradable Ag –Persistent / nondegradable Ag –
lymphocytes are replaced by macrophageslymphocytes are replaced by macrophages
over 2 -3 weeks -- epithelioid cellsover 2 -3 weeks -- epithelioid cells
 GranulomaGranuloma – microscopic aggregate of– microscopic aggregate of
epithelioid cells surrounded by collar ofepithelioid cells surrounded by collar of
lymphocyteslymphocytes
APR-2015-CSBRP

58. Classic delayed type hypersensitivityClassic delayed type hypersensitivity
CytokinesCytokines
 IL-12IL-12
 IFN γIFN γ
 IL-2IL-2
 TNFTNF
APR-2015-CSBRP

59. Figure 6-21
Schematic
illustration of the
events that give rise
to the formation of
granulomas in cell-
mediated (type IV)
hypersensitivity
reactions. Note the
role played by T cell-
derived cytokines.
APR-2015-CSBRP

60. Classic delayed type hypersensitivityClassic delayed type hypersensitivity
 CytokinesCytokines
 IL-12IL-12
 Derived from macrophageDerived from macrophage
 Differentiation of CD4+ helper cell to TDifferentiation of CD4+ helper cell to THH1 cell1 cell
 Induces IFN γ secreation by T cell & NK cellInduces IFN γ secreation by T cell & NK cell
APR-2015-CSBRP

61. Classic delayed type hypersensitivityClassic delayed type hypersensitivity
 Interferon – gamma (IFN γ )Interferon – gamma (IFN γ )
 Important mediator of delayed hypersensitivityImportant mediator of delayed hypersensitivity
 Powerful activator of macrophagesPowerful activator of macrophages
 Stimulate the secretion of IL – 12Stimulate the secretion of IL – 12
 Express more class II molecule on the surfaceExpress more class II molecule on the surface
 ↑↑ capacity to kill micro organism/tumour cellcapacity to kill micro organism/tumour cell
 Secretes PDGF & TGF – β -- stimulateSecretes PDGF & TGF – β -- stimulate
fibroblast proliferation - fibrosisfibroblast proliferation - fibrosis
APR-2015-CSBRP

62. Classic delayed type hypersensitivityClassic delayed type hypersensitivity
 IL – 2IL – 2
 Autocrine & paracrine proliferation of T cellsAutocrine & paracrine proliferation of T cells
 TNF – α and lymphotoxinTNF – α and lymphotoxin
 Act on endothelial cellsAct on endothelial cells
 ↑↑ secretion of prostacyclin – vasodilatationsecretion of prostacyclin – vasodilatation
 ↑↑ expression of E selectinexpression of E selectin
 Secretion of IL-8Secretion of IL-8
Overall effect is extravasation & accumulation ofOverall effect is extravasation & accumulation of
lymphocyte and monocyte at the site of reactionlymphocyte and monocyte at the site of reaction
APR-2015-CSBRP

63. Type VType V
Receptor type of Antibodies
APR-2015-CSBRP

64. Type V HypersensitivityType V Hypersensitivity
IgG antibodies against cell-surface
receptors disrupt the normal functions
of the receptor.
By causing :
- uncontrolled activation or
- by blocking receptor function.APR-2015-CSBRP

65. APR-2015-CSBRP

66. E N DE N D
APR-2015-CSBRP