Immune Response to Infections - Gatekeepers & Guards
- Innate Immunity (First Line): Rapid, non-specific.
- Barriers: Physical (skin, mucosa), chemical (lysozyme, pH), biological (flora).
- Key Cells:
- Phagocytes: Neutrophils (early), Macrophages (APC, late).
- NK Cells: Cytotoxic; target viral/tumor cells (no prior sensitization).
- Recognition & Signaling:
- PRRs (e.g., TLRs, NLRs): Detect PAMPs (Pathogen-Associated) & DAMPs (Damage-Associated).
- Complement System: Proteins activated via Classical, Alternative, Lectin pathways.
- Functions: Opsonization (C3b), Lysis (MAC: C5b-C9), Inflammation (C3a, C5a). 📌 CALM.
> ⭐ **TLR4** recognizes Lipopolysaccharide (LPS) on Gram-negative bacteria, a key PAMP.
Immune Response to Infections - Special Forces Strike
Adaptive immunity: "Special Forces" (T & B lymphocytes) for targeted elimination & memory. APCs present antigens via MHC for activation.
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Cell-Mediated Immunity (CMI): T-cell driven; combats intracellular pathogens (viruses, Mycobacteria) & tumor cells.
- CD4+ T Helper (Th) Cells: Orchestrate.
- Th1: IFN-γ → Potent macrophage activation (vs. intracellular microbes); granuloma formation.
- Th2: IL-4, IL-5, IL-13 → B-cell switching to IgE, eosinophil activation (helminths, allergy).
- CD8+ Cytotoxic T Lymphocytes (CTLs): Directly kill virus-infected/tumor cells (perforins/granzymes); MHC-I restricted.
- CD4+ T Helper (Th) Cells: Orchestrate.
-
Humoral Immunity: B-cell driven; antibodies neutralize/eliminate extracellular microbes & toxins.
- B-cells → Plasma cells → Antibodies (IgM, IgG, IgA, IgE).
- Key Antibody Actions: Neutralization, opsonization (enhances phagocytosis), complement activation.
⭐ IFN-γ, secreted by Th1 cells and NK cells, is pivotal for macrophage activation and effective clearance of intracellular pathogens like Mycobacterium tuberculosis.
Immune Response to Infections - Know Your Enemy
Host defense mechanisms are tailored to specific pathogen classes.
- Innate Immunity: Rapid, non-specific first line.
- Cells: Phagocytes (Neutrophils, Macrophages), NK cells.
- Soluble: Complement, Interferons (IFNs), Cytokines.
- Adaptive Immunity: Specific, develops memory.
- Humoral (B-cells): Antibodies → Extracellular pathogens.
- Cell-Mediated (T-cells): CTLs (cytotoxic T lymphocytes), Th1 (intracellular pathogens), Th17 (fungi, extracellular bacteria), Th2 (helminths).
| Pathogen | Key Innate Response | Key Adaptive Response |
|---|---|---|
| Extracellular Bacteria | Phagocytosis, Complement | Antibodies (IgM, IgG), Th17 cells |
| Intracellular Bacteria | Macrophages, NK cells | Th1 cells (IFN-γ), CTLs |
| Viruses | IFN-α/β, NK cells | Neutralizing Antibodies, CTLs |
| Fungi | Neutrophils, Macrophages | Th1 cells, Th17 cells |
| Parasites (Helminths) | Eosinophils, Mast cells | IgE, Th2 cells (IL-4, IL-5, IL-13) |
Immune Response to Infections - Masters of Disguise
- Microbial Evasion Strategies:
- Antigenic variation: Altering surface antigens (e.g., Influenza, HIV, Neisseria).
- Complement inhibition: Preventing opsonization/lysis.
- Resistance to phagocytosis: Capsules (e.g., S. pneumoniae), toxins.
- Blocking IFN pathways: Dampening antiviral responses.
- Establishing latency: Persisting silently (e.g., Herpesviruses, HIV).
- Immunopathology (Damage by Immune Response):
- Cytokine storm: Excessive inflammation (e.g., Sepsis, ARDS).
- Immune complex deposition: Glomerulonephritis, vasculitis.
- Molecular mimicry: Cross-reactive antibodies triggering autoimmunity (e.g., Rheumatic fever).
- Granuloma formation: Walling off pathogens, but causing fibrosis (e.g., TB).
⭐ Antigenic variation in Trypanosoma brucei involves sequential expression of variant surface glycoproteins (VSGs), enabling chronic infection by evading host antibodies.
High‑Yield Points - ⚡ Biggest Takeaways
- Innate immunity: first defense via phagocytes (neutrophils, macrophages), NK cells.
- Adaptive immunity (T/B cells): specific, long-lasting protection, immunological memory.
- T-helper (CD4+) cells: orchestrate responses, activate B cells & cytotoxic T cells.
- Cytotoxic T (CD8+) cells: kill virus-infected and tumor cells.
- Antibodies: neutralize toxins, opsonize pathogens, activate complement.
- Granulomatous inflammation: characteristic of intracellular pathogens (e.g., TB).
- Microbes use immune evasion (antigenic variation, latency) to persist.
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