3. Innate Immunity (Part 2)

Natural active immunity example

Response after natural exposure to a pathogen (e.g., chicken pox)

Artificial active immunity example

Immunity induced by a vaccine

Natural passive immunity example

Antibodies passed from mother to offspring (in utero, colostrum)

Artificial passive immunity example

Injection of antibodies from immune animal to another (e.g., tetanus antitoxin)

Natural Killer (NK) cell origin

Bone marrow (same lineage as T and B lymphocytes)

NK cell primary targets

Virus-infected cells and cancerous cells

Two important NK cell surface receptors

Activating receptors and inhibitory receptors

Activating receptor function

Engagement encourages NK cell to kill target

Inhibitory receptor function

Engagement tells NK cell not to kill ("self" recognition)

Healthy cells avoid NK killing by displaying

MHC class I molecules (identifies as "self")

How viruses evade inhibitory recognition

Alter cell surface to hide MHC class I ("inhibitor" receptors)

How NK cells kill target cells

Exocytosis (weaken target cell membrane, causing self-destruction)

NK cell role in early infection

Respond quickly to give adaptive immune system time to activate

NK cells secrete these signaling molecules

Cytokines

Complement system proteins are made by

The liver

Number of proteins in complement system

Approx. 20 different proteins

Complement system's main role

Destroy invaders and signal other immune components

Three complement activation pathways

Classical, Alternative, Lectin

Classical pathway is triggered by

Antigen-antibody complexes

Alternative pathway description

Spontaneous, antibody-independent activation

Lectin pathway description

Targeted, triggered by lectins binding pathogen surfaces

Three main outcomes of complement activation

Inflammation, Opsonization, Lysis (cell death)

Opsonization function

"Glues" pathogens for easier phagocyte ingestion

Membrane Attack Complex (MAC) function

Pokes holes in pathogen membranes, causing lysis

Four cardinal signs of inflammation (Latin)

Calor (heat), Rubor (redness), Tumor (swelling), Dolor (pain)

Fifth clinical sign of inflammation

Loss of function

Acute inflammation primary cell

Neutrophils

Subacute inflammation cells involved

Neutrophils, monocytes, lymphocytes

Monocytes become this in tissues

Active macrophages

Chronic inflammation result if pathogen persists

Granuloma or fibrosis

Excessive granulation in horses is called

Proud flesh

Body's temperature set by

Hypothalamus

Chemicals that induce fever are called

Pyrogens

Examples of pyrogens

Bacterial toxins, antigen-antibody complexes, interleukin

Four benefits of fever

Promotes lymphocyte response, optimizes enzyme function, inhibits pathogen growth, induces lethargy

Fever helps by sequestering these minerals

Zinc and iron (needed by bacteria)

Primary cause of fever should be treated, not just

Lowering the temperature