by mtoom

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Which leukocytes can produce cytokines?
All (although a leukocyte cannot necessarily produce all cytokines)
Which leukocytes can receive cytokine signals?
All can "receive" at least some (but not necessarily all) cytokines
What 4 cell types are phagocytes?
  • Macrophages
  • Monocytes
  • Neutrophils
  • Dendritic cells
What is a chemokine?
A type of cytokine that mediates chemotaxis and regulates expression of leukocyte adhesion molecules
What is a chemotactic factor?
An agent that causes leukocytes to move up its concentration gradient. Chemokines act as chemotactic factors
What activates the classical complement cascade?
Antibody-antigen complex being recognized by C1q (e.g. antibodies may include: IgG, IgM, CRP).

Also, C1q can bind directly to LPS.
What are the (6) cell types of the innate immune system?
  • Neutrophils
  • Eosinophils
  • Monocytes
  • Macrophages
  • Natural killer cells
  • Dendritic cells
Describe 5 "barrier" mechanisms of innate immune system
  • Defensins: cationic peptides that damage cell walls of pathogens
  • Skin: Prevent pathogens from entering body
  • Secretions: Digest pathogens using enzymes
  • Stomach acid: Digest pathogens at low pH
  • Cilia: Push out pathogens
Name the 2 main complement activation fragments and 4 of their effects.
Effects of C3a and C3b:

  • Chemotaxis (of neutrophils, macrophages)

  • Vascular permeability (by direct interaction with endothelium, and activation of mast cells)

  • Activate neutrophils (PMNs) and Macrophages

  • C3b - Opsonin

What are the 2 main effects of complement cascade?
  • MAC (Membrane attack complex)
  • Complement activation fragments function as opsonins
Name 3 antigen-presenting cells (APCs)?
  • Macrophages
  • Dendritic cells
  • B cells
What do APCs do?
Internalize particles, degrade them, display their particle bits on cell surface using MHC I or MHC II.
What are the other names for CD4+ and CD8+ T cells?
CD4+ Helper T cells
CD8+ Cytotoxic T cells (CTLs)
What happens once lymphocytes are activated?
They proliferate (i.e. clonal expansion)
What happens to activated B cells?
They differentiate into plasma cells, that secrete antibodies
What 2 processes do antibodies do?
1. Opsonization (increases phagocytosis rate)
2. Neutralization (coat pathogen preventing its function)
T-helper cells secrete cytokines that do what 3 things?
  • Activative
  • Promote proliferation
  • Promote differentiation
What 4 cell types use oxidative burst (i.e. production of reactive oxygen species)?
  • Neutrophils
  • Eosinophils
  • Macrophages
  • Monocytes
What phagocytic cell has a "minimal role" in killing? What does it do instead?
Dendritic cell. Instead it it activates the adaptive immune system by presenting antigens.
What cells do most of the binding to PAMPs (i.e. have many toll-like receptors)?
APCs. Of APCs, dendritic cells (DCs) have highest expression
What is the purpose of acute inflammation?
To deliver mediators of host defense to site of injury/infection.
Name the inflammatory processes that are responsible for swelling, edema, redness and heat.
  • Swelling: neutrophil infiltration, vascular leakage
  • Edema: vascular leakage
  • Redness & Heat: vasodilation, increase blood flow
What is extravasation?
Movement of leukocytes out of the circulatory system.
What cells first encounter pathogens? How do they recognize them? In what (2) ways do they respond?
Macrophages. Using PRRs (pattern-recognition receptors). They respond by (1) phagocytosing and (2) secreting inflammatory mediators (e.g. cytokines).
Name 3 types of effects of inflammatory mediators.
  • Upregulate adhesion molecule expression on endothelial cells
  • Increase vascular permeability
  • Promote chemotaxis and activation of neutrophils
What activates the kinin cascade?
Contact with the basement membrane
What does bradykinin do? (3 effects)
  • Pain
  • Increase vasodilation
  • Increase vascular permeability
What (2) things activate mast cells?
  • Complement activation fragments (C3a, C5a)
  • Toll-like receptors (binding PAMPs)
What is released from the granules of mast cells? (4 items)
  • Histamine
  • Inflammatory cytokines (IL-6, TNF-alpha)
  • Heparin
What are 2 effects of histamine?
  • Increased vascular permeability
  • Increased vasodilation
Complement protein fragments C5a and C3a increase vascular permeability by what 2 mechanisms?
  • Directly interacting with endothelium
  • Activating mast cells
Complement protein fragments C5a and C3a are chemotactic for what 2 cell types? What 2 cell types do they also activate?
  • Chemotactic for neutrophils, macrophages
  • Activate neutrophils, macrophages
What leukocyte dominates site of inflammation by about 6 hours?
What are the 3 primary steps in neutrophil extravasation? Describe the process.
  • Rolling adhesion (i.e. reversible binding)
  • Tight binding
  • Diapedesis

Neutrophils will participate in rolling adhesion that leads to increase expression of adhesion molecules. This leads to tight binding, and eventually diapedesis (i.e. when the neutrophil uses pseudopods to squeeze between endothelial cells).
What is an ICAM? What is it?
Intercellular adhesion molecule. Receptor on endothelium that neutrophils bind to for extravasation.
What is a LFA? What does it do? What is the consequence of transient binding (i.e. on rolling adhesion and tight binding)?
Leukocyte function-associated adhesion molecule. Binds to ICAM to facilitate extravasation, and is bound transiently during rolling adhesion; this leads to increased adhesion molecule expression, which facilitates tight binding.
What is neutrophil margination?
Accumulation of neutrophils on endothelial surface.
What do neutrophils do once they reach the site of infection (2 things)?
  • Secrete cytokines (e.g. TNF-alpha)
  • Phagocytose microbes
If a neutrophil reaches the site of infection and is very activated, what might it do?
Release its destructive granule into the extracellular space, causing tissue damage and increasing inflammation.
What other cells respond to the "call for help" besides neutrophils during acute inflammation?
Monocytes. When they enter tissue, they are called macrophages.
What are the 3 main systemic effects in acute inflammation? What tissues are associated with these effects? What stimulates these systemic effects?
  • Fever <- Hypothalamus
  • Production of acute phase proteins (MBL, CRP) <- Liver
  • Leukocytosis <- Bone marrow [except IL1]

Cytokines (TNF-alpha, IL1, IL6)
What are the 4 cardinal signs on inflammation?
  • Redness
  • Swelling
  • Heat
  • Pain
What infections will cause a systemic response?
Depends on microbe and host properties. Generally infections in blood. Or: certain infections, trauma.
Which inflammatory mediators cause vasodilation?
+++ Nitric oxide

+ Histamine
+ Bradykinin
Which inflammatory mediators cause an increase in vascular permeability?
+++ Nitric oxide

++ Bradykinin
++ C5a, C3a

+ IL-1
+ IL-6
+ TNF-alpha
+ Histamine
Which inflammatory mediators cause chemotaxis?
+++ C5a, C3a

+ TNF-alpha
What are the most powerful 2 anaphylactic peptides?
C3a, C5a
What molecules can function as opsonins?
CRP, C3b, antibodies
Which inflammatory mediators activate neutrophils (PMNs) and macrophages?
C5a, C3a, TNF-alpha
Which type of lymphocyte and MHC is used for exogenous antigens?
CD4+ T cells
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