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132 Cards in this Set

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What three cell-derived chemical mediators are released by both basophils and mast cells and what are their inflammatory effects?
histamine - increase vasodilation and vascular permeability

neutrophil chemotaxic factor -
attracts circulating neutrophils to site of injury

eosinophil chemotaxic factor -
attracts circulating eosinophils to site of injury
Which of the cell-derived chemical mediators cause increased vasodilation & vascular permeability? Of these, which also causes pain?
Histamine, 5-HT, Prostaglandins, & leukotrines

Prostaglandins cause pain
Which three CD mediators are mobilized by platelet activation?
5-HT, Platelet Activating Factor (duh), & Histamine
Which three CD mediators are mobilized by cell injury?
Leukotrines, PAF, & oxygen free-radicals (activated)
Which three CD mediators come from endothelial cells (EC)?
O2, PAF, NO, & Prostaglandins
What are the 2 sources for lysozomal enzymes, what are their stimuli, and what effect do they have?
Neutrophils & macrophages

Inflammatory activation

Degredation/digestion as part of phagocytosis; also some release into EC space to cause pathogen injury (also causes collateral damage)
What is the function of PAF?
Activates circulating platelets; promotes platelet aggregation; at med-hi [], causes vasoconstriction and at low [] causes profound increase in vasodilation & vascular permeability; also causes increased LEUKOCYTE ADHESION & CHEMOTAXIS
Which two CD chemical mediators come from all injured cells?
Prostaglandins & leukotrines
Which CD chemical mediator comes from Macrophages and ECs?
What effects does NO exert?
Increased vasodilation; regulates inflammation endogenously by promoting decreased platelet aggregation & leukocyte adhesion
What are the 3 major cytokines?
TNF-alpha, IL-1, & IL-6
How do the sources of TNF-alpha, IL-1, & IL-6 differ? How are they the same?
All come from activated macrophages

IL-1 & TNF-alpha both come from injured cells

Only IL-6 come from ECs

Onlyu TNF-alpha come from NK cells and Mast cells
What stimuli cause the relase of all three cytokines?
Inflammatory activation or cell injury
The systemic effects for the 3 cytokines are all the same. What are they?
Increased CRH, fever, anorexia, & increased hepatic production of acute phase proteins (ex, CRP, MBL)
Which of the cytokines are most similar?
TNF-alpha & IL-1
What are the similar local effects of IL-1 & TNF-alpha? What additional effects does TNF-alpha have?
Increased vasodilation, vascular permeability & leukocyte adhesion

TNF-alpha also attracts and activates monocytes & neutrophils and promotes macrophage phagocytosis
How do mast cells differ from basophils?
Mast cells live in tissue
What are monocytes?
Inactivated circulating cells that when activated become active macrophages
Where do t-cells mature?
What is the common progenator of blood constiuents?
Myeloid progenator
What cells come from the common lymphoid progeinator?
B-cells, t-cells, & NK cells & dendritic cells
What is the product of megakaryocytes?
What differentiates T & B lymphocytes?
The former differentiates in the thymus while the latter in the bone marrow
What do B & T cells differentiate to after encounter w/ an antigen?
antibody-secreting plasma cells & effector t-cells
What is the process that dendritic cells undergo on their way to activated macrophages?
Start in blood from myeloid progenitor cells -> goes into general blood circulation -> encounters potential pathogen -> enters lymphoid tissue -> activate antigen-specific T-cells
When do granulocytes enter tissue?
Only at sites of infection or inflammation
Which 2 granulocytes are implicated in allergic reactions and in defense against parasites?
Eosinophils & basophils
Which granulocyte is recruited to phagocytose bacteria?
Besides dendritic cells, which two leukocytes live within tissue?
Monocytes (become macrophages) & mast cells
Which cells are responsible for antigen presentation when activated? How is one different from the other?
Dendritic cells & macrophages; the former is responsible for antigen presentation only in the lymph nodes (in peripheral sites, they're responsible for antigen uptake
What is cell-mediated killing? What kind of immunity is this?
When a killer cell can tell if a cell is abnormal or infected

How do NK cells destroy cells?
Release enzymes which punch holes in target cell's plasma membrane
Which granulocyte is considered a 1st responder to inflammation?
Which cells are complimentary to mast cells?
Why are dendritic cells considered to be antigen-presenting cells?
Because they are macropinocytic (take large "gulps" of EC fluid to sample for infections
What are the properties of T-cells with a CD4 marker? CD8?
First is a t-helper cell; other is a cytotoxic T-cell
Describe the lifespan of a B-cell:
Produced in marrow -> travel through blood stream -> when activated -> undergoes differentiation to plasma cells -> these produce antibodies
What do helper T-cells do?
Mediate immune response meaning they can recognize an anti-body and activate a B-cell or cyto-toxic T-cell in response to very specific pathogen
What's the difference between NK cells and cytotoxic T-cells?
The former isn't specific
What three organs are part of the RES (reticuloendothelial system) but not the lymphoid system?
Liver, skin (langerhans cells), & connective tissue
What 2 cell types do the bulk of antigen presentation to helper-T cells?
macrophages & dendritic cells
What two organs/tissues are considered central lymphoid organs?
Bone marrow & thymus
Which lymphoid organ has direct access to blood stream and, as a result, can bypass lymphatic fluid?
What do lymphatic vessels pick up?
What are the 4 means for detecting a pathogen that has broken through epithelia?
1) Tissue phagocytic cells (macrophages/dendritic cells)

2) Peripheral lymphoid tissue phagocytes (via lymph)

3) Splenic phagocytic cells (via blood)

4) Circulating B lymphocytes
After detection, which cells initiate an inflammatory response by recruiting more of them to the the area?
After causing inflammation, what 2 routes do phagocytes use to present antigens and to what kind of cells?
Directly in lymphoid tissue/spleen


Phagocytes migrate to lymphoid tissue

T-helper cells
What do T-helper cells do when presented with an antigen? What is this response called?
Activates cytotoxic T-cells and B lymphocytes

Adaptive immune response
What are the 3 areas of a lymph node and what are their primary constiuents?
Medullary: phagocytic cells

Paracortical: t-cells
Why do lymph nodes have multiple zones?
To better trap antigens
What are germinal centers in lymph nodes?
areas of very rapid proliferation of whichever specific lymphocyte that’s been IDed
What are the 2 functional zones of the spleen called? What function do they serve?
Red Pulp: traps aging RBCs

White Pulp: clustered around arterioles; contain lymphocytes
What mediate transmission bet immune cells?
What are the two lines of innate defense?
Epithelial barriers (physical & chemical

Inflammatory response
What are the hallmark signs of acute inflammation?
swelling (edema), redness (erythema), heat, & pain (algesia)
What 2 main purposes does the inflammatory response have in the immune response?
Isolates area of injury

Helps to deliver WBCs to injury by enlarging blood vessels -> endothelial cells further apart -> leaks -> phagocytes able to enter
What are the 4 main steps in the inflammatory response?
1) Histamine released by damaged tissue, increasing bloodflow to area of injury

2) Histamines cause capillaries to leak, releaseing phagocytes & clotting factors into wound

3) Phagocytes engulf debris and dead cells

4) Platelets move out of capillary to seal wounded area.
What 2 types of events occur in inflammatory process?
Vascular changes/events & Cellular events
What are the 2 main components of Vascular Events and their mechanisms? What is the 3rd delayed event?
Vasodilation (heat & redness) & increased permeability of microvasculature (more space in Endoth cells -> more plasma proteins leak out -> loss of IC fluid volume -> increase in osmotic pressure -> edema)

Vascular stasis (blood more viscous -> reduced flow in vessel
What are the 4 cellular events in inflamm. response, what cells are affected, and when do they occur?
1)Circulating WBCs are stimulated to migrate to site of injury

2) These then adhere to the endothelial lining at the site of injury

3)They then squeeze themselves in between endothelial cells and undergo transmigration (cells that are squeezing through those endothelial cells) and get outside of the vessel; once outside, they start to detect pathogens in the ECF since bacteria in particular

4)They then undergo hemotaxis (move in the direction of the bacteria because the bacteria release a chemical signal) and then destroy the bacteria; these are generally phagocytes (neutrophils)


Can occur same time as vascular
4 overlapping pathways for inflammatory response?
1) Injured tissue releases cytokines that activate macrophages

2) Injury activates Mast Cells (mast cells release pro-inflammatory mediators)

3) Macrophages detect/ingest pathogen then release pro-inflammatory mediators

4) Activated macrophages stimulate Mast cells to release pro-inflammatory mediators)
What kind of response is there for pathogens that get by epithelial border but don't cause tissue injury?
pathogen alone can activate an inflam response via phagocytosis and the subsequent release of cytokines
1st cells that initiate inflammatory response?
Tissue mast cells and tissue macrophages
Which cytokine can activate mast cells?
What are the 2 mediators released by mast cells?
First is via degranulation (similar to exocytosis); secretory granules inside are released when activated; a big component released is Histamine (a very potent vasodilator and vastly increases permeability)

Second is release of newly synthesized Leukotrienes and prostaglandins, which is a delayed response (these are arachodonic acid products)
Activation pathways for mast cells?
direct injury; IL-1; IgE-mediated mechanisms (anti-body); activated complement system (composed of plasma proteins that is a very important part of innate immunity and can initiate inflammatory response through activation of mast cells)
Circulating equivalent for mast cells?
What effect does vasodilation have in inflam response that is beneficial?
Increases fluid allowed in microvasculature which contains lots of leukocytes
What causes release of albumin into IS space by endothelial cells?
More permeable -> retraction of cells -> bigger gaps -> leaks
When does vascular stasis occur?
When a critical mass of neutrophils and eosinophils have migrated to site of injury
What function does leukocytic adhesion have?
prevents leukocytes from getting swept up into general circulation
What happens after leukocytes adhere to EnC?
Transmigrate to IS where they "sniff" out pathogens -> phagocytize pathogens -> extra fluid swept up into lymphatic circulation
What are the constiuents of plasma protein systems?
enzymes that become activated, resulting in a chain rxn
How is 5-HT released?
Cytokines/tissue injury -> activation of platelets -> 5-HT release (similar axn to H1)
Besides activating more platelets, what else do PAF do?
Mediate many other inflam responses (adhesion, etc.)
Where do Lysozomal enzymes act, and where they do they reside?
They can act either IC or EC:

IC: They sit in macrophages and allow them to digest pathogens when phagotycized

EC: released to kill neighboring pathogens (results in collateral damage)
What is opsonization and what system is it related to?
Tagging of pathogens to make them more attractive to phagocytes

Complement System activation
What are the 3 ways to activate the complement system?
1 – The presence of a pathogen

2 – As part of a systemic inflammatory response

3 – Can be activated by adaptive immunity (antibody-mediated)
What is the most potent activator of clotting cascade?
Exposed collagen
What are the 3 outputs of the complement system?
1) More inflammation

2) Opsonization

3) Creates memmbrane attack complex
What does Kinin system activation cause?
Activation of Complement System
Steps from presence of pathogen to Complement activation?
Macrophage activation -> inflammation -> migration of neutrophils -> activates Kinin system
Tissue injury pathways?
Clotting cascade activation (blood clotting & pain) -> Kinin cascade activation (pain & clotting) -> Complement activation -> inflammation
Three pathways of complement activation?
Classical, MB (mannose-binding lecithin), and Alternative pathways
Classic pathway mechanism? How does binding occur?
Classic pathway involves the binding of the first protein of a complement system to the pathogen surface, which can then cause the cascade;

binding can happen directly,

via CRP (a systemic marker of inflammation) which is then bound to pathogen surface,

and the antibody-antigen complex, where a specific (i.e. B-cell) response can turn on the complement system which is part of an adaptive response
MB-L pathway mechanism?
C1q binds to mannose-binding lecithin -> bound to pathogen surface
Alternative pathway mechanism?
complement system bypasses the first two complement proteins, causing C3 to bind directly to pathogen surface
Crucial step in all 3 pathways for Complement system?
C3 convertase
What are inactive circulating kinins called?
What is kallikrein? What are the two ways of producing?
Liberate kinins from kininogens

Neutrophil activation & Factor XII activation
Ultimate purpose of clotting cascade?
To convert fibrinogen to fibrin, which forms clots
What is thrombin?
pro-inflammatory contributor
Main player in clotting cascade?
Factor XII
Clotting cascade activation?
Activated platelets, tissue damage, or both
When does a Systemic inflammatory response occur? What is this response called?
when you have enough of the inflammation mediators (especially cytokines) to bind systemically to different tissues

Acute-phase response
Which cytokine is a major mediator of sepsis when high levels occur for global effects?
Where does a large effect from an acute-phase response occur?
Bone marrow
What happens to cortisol levels during an acute-phase response?
What happens to hepatic protein production during APR?
Rate of production of ARP proteins (CRP & MBL) increases; that of other proteins decreases
What kind of nuclear material is always present in viral ifx?
double-stranded RNA
What does interferon do?
Signals viral infections
What effects do interferon have?
Producing cell: stimulates host cell that degrade viral RNA & block viral protein production)

EC: activates NK cells to attack infected cells and causes the NKs to produce interferon-gamma
What does interferon-gamma do?
Increases effects of interferon- alpha & -beta
Where do you find MHC I molecules? MHC II?
All cells in body (except for RBCs)

Antigen presenting cells (macrophages, dendritic cells, B cells)
What cells recognize MHC I cells? MHC II?
cytotoxic-T cells & NK cells

helper T-cells
Which MHC cells are involved in adaptive immune response?
What do MHC I cells ix?
virus infected, non-self, or abnormal self cells
How is adaptive immune response activated?
by recognizing non-self and missing-self antigens
What type of immunity are B-cells involved in and what do they create?
Humoral immunity

Antibodies (Ig)
Where does generation of clonal diversity occur?
central lymphoid organs
B-cell differentiation?
Triggered by matching antigen -> engulfs antigen and displays fragments bound to unique MHC -> combo of MHC & antigen attract mature matching helper-T -> T releases cytokines -> B cells multiply & mature into plasma cells -> released into blood
Antigen Presenting Cell in naive lymphocytes?
Dendritic cells
Where do B-cells recognize antigens? T-cells?
Outside cells of the body

Inside infected cells of the body
Requirements for clonal selection of t-cells?
Must be reactive and specific to MHC or peptide molecules
Major function of all IgG subtypes:
Diffusion into extravascular sites
Ig subtypes that activate complement systems?
IgM & IgG3
Function of IgE?
Sensitization of mast cells
Ig neutralizers?
IgGs & IgA
Ig for transport across epithelium?
IgA (dimer)
Ig for opsonization? & sensitization for killing by NK cells?
IgG1 (lesser extent, IgG3
Arachidonic acid metabolites in inflammation?
COX (prostaglandins [prostacyclin & thromboxane)

Lipoxygenase (lipoxin A & B)
Negative selection in clonal selection:
Forces lymphocytes to try to bind to self-peptides; those with high affinity die
Plasma cells are created when:
B-cells phagocytize a pathogen -> B-cell becomes APC -> antigenic peptides loaded into MHC II on EC surface -> helper-T binds to MHC II/antigen site -> B-cells activated -> plasma cells
Killer T's work by:
punching holes in infected cell, causing apoptosis
Killer T's only recognize antigens coupled to:
MHC I molecules
Helper T's and B's only recognize antigens coupled to:
MHC II molecules
Class switching occurs in ______. The resulting cells can now interact with different _______ molecules but retain the same binding affinity for antigens.
mature B-cells

Effector cells:
have been activated by their cognate antigen, and are actively involved in eliminating a pathogen
Exogenous antigens are usually presented by"
Dendritic cells
IgE cells cause Type I rxns because:
They are marked by B-cells, which make large amts of IgE specific antibody, resulting in a memory rxn on subsequent exposure
What does MBL do?
recognizes carb patterns as 1st line of defense
What does CRP do?
assists in complement binding