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41 Cards in this Set

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why do leukocytes migrate?
becasue they are the effector cells of inflammation
purpose of leukocyte circulation:
to increase the chance of an antigenically committed cell encountering its intended antigen
What are the circulation routes of NAIVE lymphocytes?
after 30 min in the blood, exit to the lymph nodes via High endothelial venules; if no antigen encounter, exit the efferent and back to the blood
what is the circulation pattern of EFFECTOR cells (lymphocytes) including memory cells?
45% go to the spleen
10% go to 3iary lymphoid tissue - Mocsal epithelia, liver, brain, and skin
What activates leukocyte migration?
inflammatory mediators (cytokines, anaphylatoxins, etc)
2 factors that determine WHEN and WHERE leukocytes will circulate:
Cell-adhesion molecules (homing)

Inflammatory mediators
4 types of cams:
Selectins
mucins
integrins
immunoglobulin superfamily ICAM
how do inflammatory mediators activate extravasation?
upregulate cell-adhesion molecules of endothelial cells
Which specific inflammatory mediators activate extravasation?

By what mechanism do they activate?
C3a, chemokines


1. Activate endothelium to upregulate addressins - cams
2. Activates white blood cells
3. Chemotactic - directs WBCs to the inflammatory site
4 steps of Extravasation:
1. Rolling - CAMs tether the neutrophil lightly to slow it down.
2. Activation - the endothelial cell secretes chemokines, makes neutrophil integrin bind tight to ICAM.
3. Arrest/adhesion - cells bind togheter
4. Transendothelial migration - neutrophil migrates to tissues.
What are the roles of chemokines and extravasation?
chemokines direct WBC migration to tissues during inflammation.

they also direct WBC to the proper inflamm. site after extravasion.

binding to WBC chemokine receptors causes ameboid shape for trans migration. can induce granule formation
what are the roles of chemokine receptors in WBC extravasation?
Different leukocytes express different chemokine receptors.

Only will bind if they possess the proper receptor; allows differential migration of cells to intended places.

DIRECTING TRAFFIC
what is the important difference between the otherwise similar neutrophil and lymphocyte extravasation?
Lymphocytes HOME to differential sites.

process: Trafficking
what are homing receptors?
chemokine receptors on lymphocytes that bind specific chemokines to cause specific direction of lymphocyte trafficking to lymphoid and inflamm. tissues
where do homing receptors cause naive lymphocytes to recirculate to?

Why
2ndary lymphoid tissue:
peyer's patches, lymph nodes, tonsils, spleen.

for activation by interaction with Ag
What are high-endothelial venules?

what is the purpose of these HEVs?
special regions of plump, cuboidal cells in postcapillary venules of lymph nodes.

Major site of extravasation from circulation into the lymph node.
Why/when do HEVs develop?
in the presence of cytokines produced in response to captured antigen.
How do naive cells know to go through HEVs?
HEVs express vascular addressins - special cell adhesion molecules that bind naive cells and direct them to secondary lymph organs and tissue.
major difference between neutrophil and naieve/effector lymphocyte extravasation:
different cell adhesion molecules direct trafficking
4 cardinal symptoms of inflammation:
red, heat, pain, swelling
7 mediators of inflammation:
Bradykinin
Clotting system
fibrinolytic system
complement system
histamine
leukotrienes/prostaglandins
cytokines
what are the 4 plasma enzyme mediators of inflammation:
bradykinin
clotting
fibrinolytic
complement
purpose of bradykinin:
induces pain
purpose of clotting:
acts on fibrinogen to form clots - barrier to infection spread
purpose of fibrinolytic system
plasmin - breaks down clots; these can activate complement
purpose of complement
produce anaphylatoxin to cause mast cell degranulation and chemotaxis
how are leukotriene and prostaglandin derived?
from arachidonic acid, which is from membrane phospholipids. this is induced after conjugate formation of target cell and granulytic cell
purpose of histamine
potent mediator of inflammatory response; increases vasodilation, vascular permeability, smooth-muscle contraction
what activates a local inflammatory response?
inflammatory mediators released at the site of invasion
4 steps in local inflammatory response:
1. tissue damage or bacteria can activate complement and bradyinin/plasmin/fibrin.

2. mediators cause upregulated CAMs on vascular endothelium

3. Neutrophilsl extravasate.
4. Activated neutro upregulate chemokine receptors; chemotaxis occurs.
5. ROI/RNI and upreg. granules for killing of pathogens
symptoms of local inflammation:
red, hot, pain, swelling/edema
what is the acute systemic inflamm. response, and why does it occur?
accompanying response to local infl.;
Macrophages at local site secrete cytokines; causes:
Fever from hypothalamus,
leukocytosis in bone marrow,
corticosteroids from hypothalamus,
activation of complement by acute phase proteins -> mannose-binding and c-reactive protein.
Purpose of systemic acute-phase response:
to activate complement, even though this is still INNATE response; allows efective elimination of pathogens
what causes a chronic inflammatory response?
persistent presence of antigen due to
-bacterial evasion of phagocytosis
-Autoimmune disorder - self cells are seen as antigen
what is the hallmark of chronic inflammation?
accumulation of activated macrophages
what are the symptoms of chronic inflammation?
-Fibrosis - scar tissue formation
-too much HEV from cytokine overstim.
-Granuloma - secretes more cytokines
-Epitheloid cells - fused giant multinucleated macrophages.

Chronic WASTING
What are some chronic inflammatory diseases?
-Crohn's disease ( maybe )
-Rheumatoid arthritis
-tooth cavity

can be any tissue damage
2 main symptoms of chronic inflamm. that make it self-perpetuating:
1. HEV-like vasculature near inflam. site causes perpetual inflammation.
2. Continual production of inflammatory mediators causes chronic wasting.
3 mechanisms for preventing inflamation:
1. block CAMs with antibody
2. corticosteroid treatment
3. NSAIDS (nonsteroidal) inhibits production of prostaglandin/leukotriene
by what mechanism do corticosteroids stop inflammation?
-cytotoxic to lymphocytes
-lipophilic; allows entrance of cells to alter functions, decrease inflamm. processes
-inhibits phagocytic activity
what does leukotriene cause?
smooth muscle contraction