Give diagrammatic scheme of type 2 hypersensitivity reaction with name related to it
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Here is a complete, well-sourced breakdown of Type II (Antibody-Mediated / Cytotoxic) Hypersensitivity with both diagrammatic schemes from authoritative textbooks:
Type II Hypersensitivity - Antibody-Mediated (Cytotoxic) Reaction
Also known as: Antibody-Dependent Cytotoxic Hypersensitivity
KEY CONCEPT
Antibodies (IgG or IgM) directed against antigens on cell surfaces or extracellular matrix cause cell destruction through three main mechanisms.
DIAGRAM 1 - Mechanisms of Antibody-Mediated Injury (Robbins Pathology)
Fig. 6.16 from Robbins & Cotran Pathologic Basis of Disease
DIAGRAM 2 - Antibody-Dependent Cytotoxicity (Roitt's Essential Immunology)
Figure 14.15 from Roitt's Essential Immunology
SCHEMATIC OVERVIEW
ANTIGEN on Cell Surface / Extracellular Matrix
|
▼
IgG / IgM Antibody Binds
|
┌─────────┼──────────────┐
▼ ▼ ▼
MECHANISM A MECHANISM B MECHANISM C
Opsonization Complement Antibody-Mediated
& Phagocytosis Activation Cellular Dysfunction
| | |
▼ ▼ ▼
Fc receptor C1→C3→C5 Anti-receptor
on phagocyte activation antibody
| | |
▼ ┌────┴────┐ ▼
Phagocytosis ▼ ▼ Blocks/stimulates
of opsonized C5a→ C5b-9→ normal receptor
cells Neutrophil MAC function
recruitment |
↓ ▼
Inflammation Cell Lysis
Tissue Injury
THREE MECHANISMS IN DETAIL
A. Opsonization & Phagocytosis
- Antibody coats (opsonizes) the cell
- Phagocytes recognize via Fc receptors (IgG) or C3b receptors (complement)
- Cell is ingested and destroyed
- Mainly occurs in the spleen
B. Complement Activation + Inflammation
- IgG/IgM binds antigen on cell or tissue
- Classical complement pathway activated: C1 → C4 → C2 → C3
- C3 cleaved into C3b (opsonin) + C3a (anaphylatoxin)
- C5 cleaved into C5a (chemotaxis, anaphylatoxin) + C5b
- C5b-C9 forms MAC (Membrane Attack Complex) → cell lysis
- C5a attracts neutrophils → degranulation → tissue injury
C. Antibody-Dependent Cellular Cytotoxicity (ADCC)
- Target cells coated with IgG are killed by NK cells, monocytes, neutrophils, eosinophils
- Effectors bind via FcγR receptors (not phagocytosis)
- Extracellular killing - important for large targets (parasites, tumors)
DISEASES ASSOCIATED WITH TYPE II HYPERSENSITIVITY
| Disease | Target Antigen | Mechanism | Manifestation |
|---|---|---|---|
| Autoimmune Hemolytic Anemia | RBC membrane proteins | Opsonization + phagocytosis | Hemolysis, anemia |
| Hemolytic Disease of Newborn (Erythroblastosis fetalis) | Rh antigen on fetal RBCs | Maternal IgG crosses placenta, destroys fetal RBCs | Fetal anemia, jaundice |
| Transfusion Reaction (ABO mismatch) | ABO blood group antigens | Complement lysis + phagocytosis | Acute hemolysis |
| Autoimmune Thrombocytopenia | Platelet GpIIb:IIIa integrin | Opsonization + phagocytosis | Bleeding |
| Goodpasture Syndrome | Collagen IV in GBM and alveoli | Complement + Fc-mediated inflammation | Nephritis, lung hemorrhage |
| Myasthenia Gravis | Acetylcholine receptor (NMJ) | Antibody blocks receptor; complement injury | Muscle weakness, paralysis |
| Graves' Disease | TSH receptor on thyroid | Antibody stimulates receptor (mimics TSH) | Hyperthyroidism |
| Pemphigus Vulgaris | Desmoglein (epidermal junctions) | Protease activation, loss of cell adhesion | Skin bullae |
| Acute Rheumatic Fever | Streptococcal Ag cross-reacts with myocardial Ag | Inflammation, macrophage activation | Myocarditis, arthritis |
| Pernicious Anemia | Intrinsic factor (gastric parietal cells) | Neutralization of IF → ↓ Vit B12 absorption | Megaloblastic anemia |
KEY POINTS FROM YOUR NOTES (Confirmed)
- RBCs have intrinsic Ag on surface - correct (e.g., ABO, Rh antigens)
- B cells & T cells get activated - B cells produce the IgG/IgM antibodies
- IgG/IgM production - the effector antibodies of Type II
- C3, C3b, C5 - complement cascade cleavage products
- C5a, C4a, C5a attract neutrophils - chemotactic fragments
- Neutrophils are cytotoxic to cells via degranulation
- Type II = Hypersensitivity rxn - confirmed
- Examples noted: Rheumatic fever, Erythroblastosis fetalis, petty (petechiae in ITP)
Sources: Robbins & Cotran Pathologic Basis of Disease (Fig. 6.16); Robbins & Kumar Basic Pathology (Table 5.4); Roitt's Essential Immunology (Fig. 14.15)
Make diagramatic scheme from my information only no extra
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Here is the diagram built strictly from your notes. Here's what was included, exactly as you wrote:
Image 1 (page 1) notes used:
- RBCs have intrinsic Ag on their surface
- B cells & T cells get activated
- Production of IgG / IgM
- IgG / IgM activated
- First C1, C2 is adopted → they bind to Fc region of Ab
- Family of proteins that work via complement system (lysis + destroying mechanism)
- Also known as: Hypersensitivity (Type-2) / Humoral-complex mediated
Image 2 (page 2) notes used:
- C3 → C3b → C5 → C5b-C9 (cleavage)
- C5a, C4a, C5a → attract neutrophils
- They are cytotoxic to cells → tissue damage → autoimmune reactions → Type II Hypersensitivity Rxn
- Neutrophils = RBC lysis
- Examples: Rheumatic fever, Erythroblastosis fetalis, Petty (ITP)
- Motion Ab → Petty / Haemolytic anaemia
Nothing extra was added - only your written content.
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