Explain each and every line with reasons with details like you are giving a lecture. Also explain complicated terms that are written here explain as explain to non medico
| Topic | Key Point |
|---|---|
| IgG | Most abundant, crosses placenta, warm AIHA, fixes complement |
| IgA | Mucosal guard, secretory component, breast milk, dimer in secretions |
| IgM | First responder, pentamer, cold AIHA, B cell receptor |
| IgD | Surface of naive B cells only |
| IgE | Allergy + parasites, binds mast cells, cross-links with allergen |
| Complement Classic | IgG/IgM triggers → C1→C4→C2→C3 |
| Complement Alternative | Bacterial surface triggers directly |
| Complement Lectin | Mannose on bacteria → MBL-MASP |
| MAC (C5b-9) | Drills holes in gram-negative bacteria |
| C3b | Opsonin - coats bacteria for phagocytosis |
| C1-INH deficiency | Hereditary angioedema, ↓C4, ACE-I contraindicated |
| PNH | PIGA mutation → no GPI → RBCs attacked by complement → dark urine |
| IL-1 | Fever, acute inflammation |
| IL-6 | Fever, acute-phase proteins |
| TNF-α | Cachexia, granulomas (TB), sepsis |
| IL-8 | Neutrophil chemotaxis |
| IL-12 | Th1 differentiation, NK activation |
| IFN-γ | Macrophage activation, kills intracellular pathogens |
| IL-4 | Th2 differentiation, IgE/IgG class switch |
| IL-5 | Eosinophils, IgA |
| IL-10 | Anti-inflammatory |
| Respiratory burst | NADPH oxidase → superoxide → H₂O₂ → HOCl |
| CGD | NADPH oxidase defect → catalase+ infections (S. aureus) |
| IFN-α/β | Antiviral, downregulate protein synthesis, used in HBV/MS |
| Type I | IgE, mast cells, histamine, immediate allergy |
| Type II | IgG/IgM attack cells (Graves, MG, hemolytic anemia) |
| Type III | Immune complexes, complement, neutrophils (SLE, serum sickness) |
| Type IV | T cells only, DELAYED (contact dermatitis, PPD, GVHD) |