Non-Adaptive Immunity
Includes intrinsic and innate defenses.
Same response for all pathogen types.
Adaptive Immunity
Specific responses for each microorganism.
First Line: External body membranes (skin and mucosae).
Second Line: Antimicrobial proteins, phagocytes, and other cells; inflammation is key.
Characteristics:
General response system functioning the same way, eliminating almost all pathogens.
Does not identify individual pathogens.
Attacks particular foreign substances, slower to react.
Adaptive system tailors its response to individual pathogens.
Innate and adaptive defenses are intertwined.
Skin, mucous membranes, and secretions act as physical barriers.
Keratin resists acids, bases, bacterial enzymes, and toxins.
Mucosae provide similar mechanical barriers.
Inhibit or destroy microorganisms.
Skin acidity.
Lysozyme in saliva and lacrimal fluid.
Mucus.
Always present in uninfected cells; includes:
Apoptosis.
Autophagy.
RNA silencing.
Antiviral proteins.
Programmed cell death; intrinsic (self-initiated) and extrinsic (induced by external signals).
Neutrophils undergo apoptosis after about 1 day.
Mechanism bacteria use to edit their DNA after virus insertion.
Pathogen attaches to multiple host receptors, triggering a specific immune response.
Non-adaptive immunity uses cell receptors that recognize pathogen-associated molecular patterns (PAMPS).
Secreted proteins that kill bacteria or infected host cells after patterned attachment signals.
Attacks pathogens without specificity, acts quickly.
Cells and proteins needed if microorganisms invade deeper tissues.
Antimicrobial proteins (interferons and complement proteins).
Inflammation/Fever.
Ingest and eliminate infectious agents; present antigens.
Attracted by chemicals from dying cells.
Specialized for antigen presentation and T-cell activation (adaptive immunity).
Migrate to lymphoid organs with antigen.
T-lymphocytes: seek and destroy.
B-lymphocytes: produce antibodies.
Specific MHC protein matches the original antigen absorbed by the cell and moves to the cell surface.
MHC attachment programs the cytotoxic T-Lymphocyte (CTL).
Recognize normal vs. low "self" protein (MHC) levels.
Release perforins (punch holes) and granzymes (induce apoptosis).
TCR function is recognition, and CD28 is activation.
Become phagocytic upon encountering infectious material.
Release toxic chemicals and induce intrinsic apoptosis.
Release substances (e.g., histamine) contributing to inflammation.
Important in allergic responses and innate immunity.
Antihistamines: competitive inhibitors of histamine receptors.
Interferons (IFNs) and complement proteins.
Attack microorganisms or hinder reproduction.
Signal response to viral and some cancer infections.
Induce antiviral proteins in host cells.
Guide NK cells to release perforin and stimulate macrophage consumption.
Cause flu-like symptoms.
Proteins circulating in the blood in an inactive state.
Play a role in inflammatory responses.
Create osmotic imbalance.
Antibodies activate complement.
Response of vascular tissue to injury or infection.
Seeks to destroy injurious agents and confine them.
Sequence of events:
Histamine release, capillary widening, increased permeability, leukocyte attraction, fever.
Triggered by bacterial endotoxins.
Positive Effects: Stimulates phagocytosis, slows bacterial growth.
Negative Effects: Extreme heat, enzyme denaturation (above 39°C is dangerous).
Moderated by the medulla oblongata.