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A&P 2 Innate and Adaptive Immunity Terms in this set (46) Immunity resistance to disease consist of two systems 1. Innate immunity: non-specific defense system. 2. Adaptive immunity a specific defense system. innate immunity The responses releas€7,37
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A&P 2 Innate and Adaptive Immunity Terms in this set (46) Immunity resistance to disease consist of two systems 1. Innate immunity: non-specific defense system. 2. Adaptive immunity a specific defense system. innate immunity The responses releas
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A&P 2 Innate and Adaptive Immunity
Terms in this set (46)
Immunity resistance to disease consist of two systems
1. Innate immunity: non-specific defense system.
2. Adaptive immunity a specific defense system.
innate immunity The responses release proteins that alert cells of the ad...
A&P 2 Innate and Adaptive Immunity
Jeremiah
Terms in this set (46)
resistance to disease consist of two systems
Immunity 1. Innate immunity: non-specific defense system.
2. Adaptive immunity a specific defense system.
The responses release proteins that alert cells of the adaptive system to foreign
molecules and antigens. The innate defense system has two lines of defenses.
1. External body membranes, like skin and mucosae
innate immunity 2. Antimicrobial proteins (interferons and complement proteins), phagocytes
(neutrophils and macrophages), NK, that inhibit the spread of invaders. Also uses fever
and inflammatory responses (macrophages, mast cells, WBCs and inflammatory
chemicals)
1. Surface barriers for warding of invading pathogens think of skin, mucous membranes,
and their secretions.
-The physical barrier keeps out most microorganisms
-keratin is resistant to weak acids and bases, bacterial enzymes and toxins
-mucosae provides similar mechanical barriers
2. Protective chemicals used to inhibit or destroy microorganisms.
-The acidity of skin and secretions inhibits growth
Innate immunity defenses -enzymes or lysosomes of saliva, respiratory mucus, and lacrimal fluid kill many
microorganisms
- defensins like antimicrobial peptides that also inhibit growth
-other chemicals think of lipids in sebum or dermicidin in sweat they are both toxic
3. Respiratory system modifications.
-mucus coated hairs in the nose help to catch bacteria
-Cilia of the upper respiratory tract sweeps, dust, and bacteria related mucus towards
the mouth away from the lungs
neutrophils: most abundant, but die fighting
Macrophages: develop from a monocyte is the chief phagocytic cell
- free macrophages wander through the tissue spaces (alveolar macrophages)
- fixed macrophages permanent residence of some organs (brain microglia)
Steps of phagocytosis
Innate immunity phagocytosis 1. The phagocyte adheres to the pathogen. This is where opsonization occurs (the
marking of the pathogen by coating it in complement proteins or antibodies)
2. The phagocyte forms pseudopods that eventually engulf the particles forming a
phagosome.
3. Lysosomes fuse with the phagocytic vesicles forming a phagolysosome
4. Lysosomal enzymes digest the particles leaving a residual body.
5. Exocytosis of the vesicle removes indigestible and residual material.
Attack cells that lack "self" cell-surface receptors like infected or cancerous cells
(similar to T cells but lack antigen receptors)
natural killer cells (NK cells)
They then induce apoptosis and secrete potent chemicals that enhance inflammatory
response
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Triggered whenever body tissue is injured and prevent the spreading of damaging
agents it disposes of cell debris and pathogens and alerts the adaptive immune system.
It also sets the stage for repair.
Signs of acute information:
Inflammatory responses 1. Redness (due to the blood flowing to the region)
2. Heat (due to all the metabolic active happening at the sight).
3. Swelling/Edema (due to increased blood flow to sight)
4. Pain. (Due to the swelling as it crushes the nearby nerves)
5. Impairment of function (due to the swelling and crushing of nerves)
It begins with chemicals like histamine released by mast cells being released into the
ECF by injured tissues, setting off the chemical alarm macrophages and epithelial cells
of the injured tissue also release cytokines that promote inflammation
Inflammatory mediators, like histamine, kinins, prostaglandins, and complement proteins
cause the local arterioles to dilate (hypermia) which leads to the redness and heat of
Triggering an inflammatory response
the inflamed region, and makes the capillaries leaky which attracts leukocytes to the
area, which also have an inflammatory role.
The increased capillary permeability leads to: local swelling this swelling pushes on
nerve endings, causing pain. Also leads to the delivering of clotting proteins in
complement proteins, clotting factors which formed the fiber mesh the scaffolding for
repair and isolates the injured area so invaders cannot spread.
-Neutrophils flood area first and die fighting; macrophages (coming from monocytes)
follow and replace the dying neutrophils
-If inflammation is due to pathogens, complement is activated; adaptive immunity
elements arrive
1. Leukocytosis: the release of neutrophils from bone marrow in response to a
Phagocyte mobilization leukocytosis-inducing factor from injured cells.
2. Margination: neutrophil cling to walls of capillaries in inflamed area in response to
CAMs (cell adhesion molecules, molecular Velcro)
3. Diapedesis- neutrophils flatten and squeeze out of capillaries.
4. Chemotaxis- inflammatory chemicals called chemotactic agents promote positive
chemotaxis of neutrophils (neutrophils follow chemical trail)
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