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Reading assignment:
Chapter 20 & 21
(Thibodeau & Patton
Anatomy
& Physiology) |
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ACT
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Interactive
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GA |
Gray's Anatomy |
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Animation |
pp |
PowerPoint
slide |
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FIG
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Figure |
term |
Define,
pronounce |
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Online previews:
Lymphatic System
Immune System
(Previews are found at
WebCT)
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Lymphatic System
General
structure and function
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Part of "circulatory
system" |
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Principal organs/tissues
pp
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Lymph (lymphatic fluid) |
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Lymphatic vessels |
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Lymph nodes and nodules |
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Tonsils |
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Thymus |
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Spleen |
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Functions
pp
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Fluid balance (returns
water, proteins, etc. from tissues back to blood) |
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Immunity |
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Transports lipids from the
digestive tract
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Lacteals (lymph
capillaries) in intestine transport fatty lymph called chyle |
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Starling's Law of the Capillaries
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In a
capillary, there are inwardly directed forces and outwardly directed forces
that are balanced or imbalanced
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Osmotic
pressure |
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Hydrostatic pressure (pressure of fluid against a membrane) |
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At the arterial end of a capillary
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Outwardly
directed forces (mostly blood pressure) causes net diffusion of water
and small solutes OUT of the blood (and into the IF
[interstitial fluid]) |
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At the venous end of a capillary
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Inwardly directed
forces (mostly tissue fluid pressure and osmotic pressure of the blood
plasma) causes net diffusion of water and small solutes INTO the blood
(and out of the IF) |
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About 10% (varies greatly) of the fluid that OUGHT to
return to the blood capillary does not
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This "extra"
interstitial fluid (IF)
in the tissue may
accumulate, causing painful swelling and potentially fatal damage to
the tissue
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Blood would also loose too much fluid to maintain
health |
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The lymphatic system includes a system of vessels
that drains this excess fluid away and returns it to the blood
supply |
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Lymphatic drainage
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Lymphatic capillaries
pp
GA
GA
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Blind-end tubules that begin in a tissue and
continue as tributaries to larger and larger vessels, like creeks
running into large streams, into rivers, into the lake |
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Lumen (hollow part) of capillaries is "always
open" like storm drainage pipe because tiny fibers attached to
surrounding tissue cells hold it open from the outside
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This allows water and small particles to drain
into the capillaries easily (without much of a pressure
gradient) |
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The drained fluid is now called
"lymph" or "lymphatic fluid" |
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Numerous SL (semilunar) valves keep lymph from
flowing back toward tissue |
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Drain away excess fluid as described above
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Also drain away fats absorbed in the digestive
tract (otherwise the fats would increase blood viscosity and
slow blood flow during absorption of a meal) |
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Lymphatic vessels and ducts
GA
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Lymphatic vessels eventually all drain into the:
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Right lymphatic duct
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drains lymph from the superior right
quadrant of body ---into the right subclavian vein (just
before the systemic blood enters the right atrium of the
heart) |
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Thoracic duct
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drains lymph from the lower right quadrant
and entire left side of body into the left subclavian vein |
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Numerous SL valves and lymph nodes (and other
lymphoid organs) |
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Lymphokinesis (kinesis =
"movement")
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One-way flow (linear;
unlike
"circular flow" of cardiovascular system) toward the
blood/heart |
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Lymphatic pump
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Similar to venous pumps |
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Lymphokinesis averages
about 125 ml/hr (that's 3 L/day) |
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| Elephantiasis
Also known as
lymphatic filariasis, this condition occurs when parasitic worms (any of
several types of filaria worms) infest the lymphatic system. The
filaria are transmitted by mosquitoes to the blood and can build a
population in the lymph nodes, blocking fluid drainage from arms, legs,
genitals, or breasts. It is called elephantiasis (literally,
"elephant condition") because in extreme cases, the arms and
legs look like the limbs of an elephant. Elephantiasis affects over a
100 million people around the world. However, most cases are not
as extreme as in this photo! |

Click to enlarge
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Lymphatic drainage of the
breasts -- a special case
GA
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Superficial lymphatics |
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Deep lymphatics |
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Lymphatic anastomoses
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Superficial with deep |
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Across median |
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With abdominal lymphatics |
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With pectoral muscles |
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Important in infections
(mastitis) and cancer (breast cancer) because bacteria or cancer cells
can easily migrate to other parts of the body, making things even more
serious |
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Lymphoid organs
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Lymphoid organs have flow-through of lymph (and/or
blood) |
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Lymphoid organs have lymphoid tissue, which is made up
of developing WBCs |
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Lymph nodes
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Each is a tiny (1-20+ mm) fibrous capsule divided into many
chambers
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Usually found in
clusters (not evenly distributed throughout body)
GA |
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Each chamber or "sinus" has may fine
(reticular) fibers suspending a lymph nodule made up of lymphoid tissue
GA
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Lymphoid tissue is
packed WBCs |
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Germinal center is the
the interior portion of a nodule
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Where B-lymphocytes
begin the last stages of development (then are released from
outer part of nodule) |
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Lymph enters node through
afferent lymphatic vessels and leaves the node through efferent
lymphatic vessels |
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As lymph flows through lymph node, lymph is
mechanically filtered by fibers (large chunks get stuck)
pp |
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Lymph is biologically filtered when phagocytes
(reticuloendothelial cells) consume the particles or otherwise attack the particles |
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Tonsils
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Three sets of lymph nodules in throat
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Pharyngeal lymphoid ring - a
protecting ring of tonsils around the entrance of digestive and respiratory
tracts
GA
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Lingual tonsils - base
of tongue |
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Pharyngeal tonsils -
posterior wall of nasopharynx (above soft palate)
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Called
"adenoids" if they become enlarged, possibly blocking
breathing |
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Palatine tonsils
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Oval thickening of
mucosa on each side of oropharynx |
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Most prominent of
all tonsils; have 10-20 pits (crypts) |
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 | Peyer's patches
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aggregated lymphoid nodules |
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wall |
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Thymus
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Also an endocrine gland, found in chest in front of
or slightly above the heart (mediastinum)
GA |
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Largest at puberty, then
shrinks slowly over time (almost gone in advanced old age [twice Kevin's
age]) |
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Cortex: lymphoid tissue
GA
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Site of T-lymphocyte (T-cell) development
(lymphocytes become T-cells under the influence of thymosin
hormones) |
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Medulla: thymic corpuscles
(function not clear; may be be where older cells
are broken down) |
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Spleen
GA
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Located in left upper part of
abdomen, under
diaphragm and tucked behind the stomach (left hypochondrium) |
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Like a giant lymph node for blood:
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Capsule with
many sinuses that contain lymphoid tissue (incl. reticuloendothelial
cells) for the filtering of blood
(including RBC/platelet destruction)
GA |
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Hematopoiesis
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RBCs (before birth) |
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Nongranular leukocytes |
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Blood reservoir |
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Immunity
Hint:
Review types of pathogens in "Mechanisms of Disease" at end
of Chapter 1 of textbook: bacteria, viruses,
protozoa, fungi, worms, etc.
Immunity is protection/defense
pp
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Often, a military warfare model is used to illustrate
immune function
pp |
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Immunity is carried out by many cells and tissues of
the body, not just those classically identified as "immune
cells" or "immune tissues" |
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Defense / protection against variety of
"enemies"
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Nonself
particles have unique identifying marker molecules
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Similar to the insignia of enemy aircraft, vehicles, soldiers |
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Self-tolerance--we do not attack our own cells |
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Examples of "enemies"
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Pathogens (see above) |
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Cancer cells (your own cells that have become
cancerous) |
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Physical damage (burns, cuts, etc.) |
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Two strategies of immunity
pp
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Innate
immunity
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Called "innate" immunity because it does not require prior exposure to a
pathogen |
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Also
called nonspecific immunity
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Mechanisms
that are "on standby" at all times and are effective against a variety
of different "enemies" |
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Innate immune mechanisms respond rapidly (always "on alert") |
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Adaptive
immunity
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Called "adaptive immunity" or "acquired immunity" because it changes to
work against new pathogens upon exposure to them |
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Also
called specific immunity
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Mechanisms that are effective
against specific (one kind only) "enemies" |
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Adaptive immune mechanisms respond more slowly because they take
time to prepare and develop |
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Note: Immunology is a complex and rapidly changing discipline. We
will be looking at a simple overview of immunology to prepare
you for further work in this area later in your studies. |
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Innate (nonspecific) defenses
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There are
many innate strategies; here we discuss just a few of them
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Many of
these innate defenses also work in cooperation with, or are
supplemented by, additional adaptive defense mechanisms |
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Species resistance |
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Lines of defense (as in military
model) |
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Surface barriers - skin and mucous membranes |
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Phagocytes - neutrophils, eosinophils, macrophages
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Antigen-presenting cells (APCs) digest the enemy particle and display
the unique protein markers to signal the adaptive immune system |
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Examples
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Macrophages = large, phagocytic cells found in many areas of the
body |
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Dendritic cells (DCs) = branched phagocytes, often at/near external
barriers |
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Natural killer (NK) cells
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NK
cells are lymphocytes that
"patrol" the body, looking for abnormal cells (esp. cancer
cells and virus-infected cells) to kill |
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NK
cells kill by direct contact with enemy cell
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NK
cells each have two receptors
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Killer-activating receptor binds to common cell markers
(thus, binds even to self cells) |
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Killer-inhibiting receptor binds to certain self markers,
thus preventing killing of self cells
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The self markers are MHC (major histocompatibility complex)
proteins unique to every individual |
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Kill by
various methods
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May
release perforins, which are proteins that form holes in the plasma membrane
of the cell to be killed
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Sodium diffuses in, then water osmoses
inward, causing the cell to swell and burst
(cytolysis) |
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In
nucleated cells, this influx of ions may
trigger apoptosis (programmed cell death), also resulting in
cytolysis |
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May
also release granzymes that can enter the cell and trigger
apoptosis
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Defensive proteins
(cytokines)
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Interferons
(IFNs) are released by dying, virus-infected
lymphocyte or other cell
pp
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Interferons "call in" other immune
cells (NK cells and macrophages) that destroy virus-infected
cells, protecting the body from further spread of viral
infection |
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Interferons also "interfere" with the
ability of viruses to replicate in other nearby cells --also
stopping the viral infection |
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Interferons are paracrine agents, regulating nearby cells |
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Complement is a group of
about 20 different plasma proteins
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Individual complement proteins are designated C1, C2, C3, and so
on |
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Complement molecules are activated in a cascade of chemical
reactions triggered by innate or adaptive mechanisms |
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Complement can act directly, as do perforins
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Form MACs (membrane attack complexes) that poke holes in the
outer membrane |
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Complement can act indirectly as a chemotactic
agent or regulating immune cells in some other way |
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Chemotaxis
pp
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Chemical attractants are released from
damaged tissue cells and immune system cells to "call over"
immune cells to the site of injury |
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Interferon activity in a virus-infected cell.
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Inflammation (the inflammatory response)
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Set of reactions in response to injury
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Four principle signs of inflammation: redness,
warmth, pain, swelling |
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Inflammation mediators are chemicals that
regulate the inflammatory response |
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Summarized in textbook
Figure 21-3 |
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Fever
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Pyrogens (literally "fire makers")
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Chemical factors released by pathogens or
immune cells |
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Causes hypothalamus ("thermostat"
of the body) to "reset" setpoint body temperature a
little higher |
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Cause liver / spleen to remove iron from the
blood, making it unavailable for pathogens |
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Mild, moderate fever increases body temp slightly
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Increases efficiency of immune mechanisms |
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Decreases efficiency of pathogen function |
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High or prolonged fever
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Can denature (change shape of) proteins, thus
disrupting enzyme activity bodywide --perhaps leading to death |
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Effector and memory cells
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Effector cells are the cells that actively
participate in "the battle" against "the enemy"
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Effector cells usually die during or just after
the "battle" |
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Memory cells are inactive copies of the effector
cells that are held as "reserves" in case the same enemy
attacks later
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Memory T cells and memory B cells can quickly
be activated or "called up to the front" and become
effector cells if the same enemy attacks again at a later time |
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Sounding the alarm
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Macrophages,
DCs, or other APCs (antigen-presenting cells)
ingest the "enemy" and incorporate the enemy markers on
the surface of the APC |
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This display of "enemy antigens" then
triggers a helper T cell (= T4 cell = CD4 cell) with complementary
receptors by releasing interleukin 1 |
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Interleukin 1 activates the helper T cell, which
divides into many identical daughter cells (the group of identical
cells is called a clone)
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Some of the cells remain inactive
"reservists" as memory helper T cells |
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