Immune Response to Infections

Immune Response to Infections

Immune Response to Infections

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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.
![Complement system activation pathways](https://ylbwdadhbcjolwylidja.supabase.co/storage/v1/object/public/notes/L1/Pathology_Immunopathology_Immune_Response_to_Infections/48181e13-0799-4a64-8f21-3631cde9749a.jpg)
> ⭐ **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.

  • 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.
  • 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.

Adaptive immune response: T-cell and B-cell 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).
PathogenKey Innate ResponseKey Adaptive Response
Extracellular BacteriaPhagocytosis, ComplementAntibodies (IgM, IgG), Th17 cells
Intracellular BacteriaMacrophages, NK cellsTh1 cells (IFN-γ), CTLs
VirusesIFN-α/β, NK cellsNeutralizing Antibodies, CTLs
FungiNeutrophils, MacrophagesTh1 cells, Th17 cells
Parasites (Helminths)Eosinophils, Mast cellsIgE, 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.

Practice Questions: Immune Response to Infections

Test your understanding with these related questions

An adult patient with a military background is admitted with a rash, fever, altered sensorium, and a deficiency of the membrane attack complex. What is the most likely etiological agent?

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Flashcards: Immune Response to Infections

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Is graft rejection humoral or cell mediated?_____

TAP TO REVEAL ANSWER

Is graft rejection humoral or cell mediated?_____

Both

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