Innate and Adaptive Immunity Flashcards

Innate vs. Adaptive Immunity

  • Time:

    • Innate: Fast response, typically within minutes post-infection.

    • Adaptive: Much slower; 2 weeks post 1st infection, 3 days after subsequent infection.

  • Recognition:

    • Innate: Recognizes stereotypical pathogen signatures (PAMPs).

    • Adaptive: Recognizes specific molecules that are specific to a pathogen.

  • Response:

    • Innate: Always present.

    • Adaptive: Requires gene arrangement.

Ports of Entry and Physical/Chemical Barriers (Innate Immunity)

  • Skin:

    • Physical: Keratin and dead cells.

    • Chemical: Low pH, salty.

  • Respiratory System:

    • Physical: Ciliary escalator, coughing, sneezing, mucus.

  • GI Tract:

    • Physical: Peristalsis (top to bottom).

    • Chemical: Lysozyme, gastric juice.

    • Anti-peristalsis: vomiting, defecation, diarrhea

  • Eyes:

    • Chemical: Tear drops, lysozyme.

  • Ears:

    • Chemical: Earwax.

  • Urogenital Tract:

    • Chemical: Urine, vaginal secretion, low pH.

First Line of Defense

Biological Factors

  • Common resident microbes serve as microbial antagonism to incoming pathogens by competing for nutrients and growth space

    • Normal flora such as E. coli produce bacteriocins which inhibits growth of salmonella

  • Probiotics - live microbial cultures applied to or other ingested that are intended to exert a beneficial effect

  • Prebiotic - chemicals that selectively promote the growth of beneficial bacteria

Natural Killer (NK) Cells Mechanism

  • Possess the ability to kill infected cells as well as tumor cells

  • Two ways to kill:

    • Perforin creates channels in the target cells, causing them to burst (cytolysis).

    • Granzymes is enzyme which digest Perforin-protein inside the target cell, inducing apoptosis of that cell

  • Normal cell: Killer-inhibitory receptor, MHC class I molecule, No attack.

  • Abnormal cell lacking MHC class I molecules: Killer-activating receptor, Kill

  • The binding of a NK cell to the target cell triggers the release of monomeric Perforins and Granzymes from the Lytic Granules (specialized vesicles in NK cells).

Identification of Pathogens by Innate Immune System

  • PAMP - Pathogen-Associated Molecular Pattern

  • PRRs (Pattern Recognition Receptor) - They receptors that can recognize PAMPs

    • TLRs (Toll-Like Receptors):

      • Membrane-bound receptors.

      • Responsible for recognizing external PAMPs.

    • NIRs (Nod-Like Receptors):

      • Cytoplasmic molecules.

      • Recognize intracellular PAMPs.

Membrane Attack Complex (MAC)

  • Regardless of which pathway the compliment sys. comes from, it leads to:

  • Pokes hole into a membrane

  • Classical Pathway – Triggered by antibodies binding to antigens, initiating a cascade that activates complement proteins.

  • Alternative Pathway – Activated directly by microbial surfaces without the need for antibodies.

  • Lectin Pathway – Initiated when mannose-binding lectin binds to sugars on the surface of pathogens, triggering complement activation.

Interferons

  • Three types: IFN-{\alpha}, IFN-{\beta}, & IFN-{\gamma}

    • IFN-{\alpha} & IFN-{\beta}: Sign for viral infection; signal to neighboring cells about infections.

    • IFN-{\gamma}: Signal for macrophages to become more effective in combating bacterial infection.

  • Mechanism:

    1. Viral RNA from an infecting virus enters the cell.

    2. The virus induces the host cell to produce interferon mRNA (IFN-mRNA), which is translated into alpha and beta interferons.

    3. Interferons make contact with uninfected neighboring host cells, where they bind either to the plasma membrane or to nuclear receptors. Interferons induce the cells to synthesize antiviral proteins (AVPs).

    4. AVPs degrade viral mRNA and inhibit protein synthesis—and thus interfere with viral replication.

Anti-Microbial Peptides (AMPs)

  • Antimicrobial peptides are short chain of amino acids (between 12 to 50), which limits certain bacterial growth.

  • Directly Kill Microbes
    *Electrostatic interaction
    *Membrane Rupture
    *Block cellular function

  • Modulate Host's Immunity
    *Recruit immune cells
    *Neutralizes bacterial products
    *Promote auto-inflammatio

  • Cathelicidin
    *Secreted by: Keratinocytes
    *Mode of action:
    *Membrane disruption

  • Polymyxin B
    *Mode of action:
    *Permeabilize bacterial outer membrane

  • Modulin
    *Produces by S. epidermidis to limit the growth of S. aureus & E. coli
    *Mode of action:
    *Bacterial Lysis
    *Secreted by: Neutrophils & other leukocytes, Epithelial cells: those lining the GI tract.