Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
127 Cards in this Set
- Front
- Back
|
What is the term for the factors whose serum concentration changes significantly in response to inflammation?
|
Acute Phase Reactants
|
|
|
Where are Acute Phase Reactants produced? When?
|
Produced in liver in both acute and chronic inflammatory states
|
|
|
What induces Acute Phase Reactants?
|
- IL-6
- IL-1 - TNF-α - IFN-γ |
|
|
What are the positive (up-regulated) Acute Phase Reactants?
|
- Serum Amyloid A
- C-Reactive Protein - Ferritin - Fibrinogen - Hepcidin |
|
|
What are the negative (down-regulated) Acute Phase Reactants?
|
- Albumin
- Transferrin |
|
|
What are the potential implications of up-regulated Serum Amyloid A during inflammation?
|
Prolonged elevation can lead to amyloidosis
|
|
|
What are the actions of C-Reactive Protein?
|
Opsonin - fixes complement and facilitates phagocytosis
|
|
|
What is a clinical measure of ongoing inflammation?
|
C-Reactive Protein (Acute Phase Reactant)
|
|
|
What are the actions of Ferritin?
|
Binds and sequesters iron to inhibit microbial iron scavenging (Acute Phase Reactant)
|
|
|
What are the actions of Fibrinogen?
|
Coagulation factor - promotes endothelial repair
|
|
|
What acute phase reactant correlates with the Erythrocyte Sedimentation Rate (ESR)?
|
Fibrinogen
|
|
|
What are the actions of Hepcidin?
|
Prevents release of iron bound by ferritin → anemia of chronic disease
|
|
|
What happens to Albumin during inflammation? Why?
|
Albumin is down-regulated → reduction conserves amino acids for positive Acute Phase Reactants
|
|
|
What happens to Transferrin during inflammation? Why?
|
Internalized by macrophages to sequester iron → down-regulated acute phase reactant
|
|
|
Which acute phase reactant fixes complement and facilitates phagocytosis?
|
C-Reactive Protein (Acute Phase Reactant)
|
|
|
Which acute phase reactant binds and sequesters iron to inhibit microbial iron scavenging?
|
Ferritin (Acute Phase Reactant)
|
|
|
Which acute phase reactant is a coagulation factor that promotes endothelial repair?
|
Fibrinogen (Acute Phase Reactant)
|
|
|
Which acute phase reactant prevents release of iron bound by ferritin?
|
Hepcidin (Acute Phase Reactant)
|
|
|
What is the system of interacting plasma proteins that play a role in innate immunity and inflammation?
|
Complement
|
|
|
What component of complement defends against gram negative bacteria?
|
MAC complex (membrane attack complex)
|
|
|
What mediates/activates the classic pathway of complement?
|
IgG or IgM (GM makes classic cars)
|
|
|
What mediates/activates the alternative pathway of complement?
|
Microbe surface molecules
|
|
|
What mediates/activates the lectin pathway of complement?
|
Mannose or other sugars on the microbe surface
|
|
|
Which complement pathway is activated by IgG and IgM?
|
Classic pathway (GM makes classic cars)
|
|
|
Which complement pathway is activated by microbe surface molecules?
|
Alternative pathway
|
|
|
Which complement pathway is activated by mannose or other sugars on microbe surface?
|
Lectin pathway
|
|
|
What are the types of complement?
|
- C3b
- C3a, C4a, C5a - C5b-9 |
|
|
What is the function of C3b?
|
Opsonization (C3b binds bacteria)
|
|
|
What is the function of C3a?
|
Anaphylaxis
|
|
|
What is the function of C4a?
|
Anaphylaxis
|
|
|
What is the function of C5a?
|
Anaphylaxis & neutrophil chemotaxis
|
|
|
What is the function of C5b-9?
|
Cytolysis by membrane attack complex (MAC)
|
|
|
Which components of complement are involved in opsonization?
|
C3b (C3b binds bacteria)
|
|
|
Which components of complement are involved in anaphylaxis?
|
C3a, C4a, C5a
|
|
|
Which components of complement are involved in neutrophil chemotaxis?
|
C5a
|
|
|
Which components of complement are involved in cytolysis by membrane attack complex (MAC)?
|
C5b-9
|
|
|
What are the two primary opsonins in bacterial defense?
|
C3b and IgG
|
|
|
What piece of complement helps clear immune complexes?
|
C3b
|
|
|
What helps prevent complement activation on self cells (eg, RBCs)?
|
Decay-Accelerating Factor (DAF, aka CD55) and C1 esterase inhibitor
|
|
|
What is the action of Decay Accelerating Factor (DAF)? Other name?
|
AKA CD55
- Helps prevent complement activation on self cells (eg, RBCs) |
|
|
What is the action of C1 esterase inhibitor?
|
Helps prevent complement activation on self cells (eg, RBCs)
|
|
|
What are the implications of a C1 esterase inhibitor deficiency?
|
Causes hereditary angioedema, ACE inhibitors are contraindicated
|
|
|
What are the implications of a C3 deficiency?
|
- ↑ Risk of severe, recurrent, pyogenic sinus and respiratory tract infections
- ↑ Susceptibility to type III hypersensitivity reactions |
|
|
What are the implications of a C5-C9 deficiency?
|
Increases susceptibility to Neisseria bacteremia
|
|
|
What are the implications of a DAF (GPI anchored enzyme) deficiency?
|
Causes complement mediated lysis of RBCs and paroxysmal nocturnal hemoglobinuria
|
|
|
What causes hereditary angioedema? What is contraindicated in these patients?
|
C1 esterase inhibitor deficiency
- ACE inhibitors are contraindicated |
|
|
What increases the risk of severe, recurrent pyogenic sinus and respiratory tract infections?
|
C3 deficiency
|
|
|
What increases the susceptibility to type III hypersensitivity reactions?
|
C3 deficiency
|
|
|
What increases the susceptibility to recurrent Neisseria bacteremia?
|
C5-C9 deficiencies
|
|
|
What causes complement mediated lysis of RBCs and paroxysmal nocturnal hemoglobinuria?
|
DAF (GPI anchored enzyme) deficiency
|
|
|
What are the important cytokines secreted by macrophages?
|
- IL-1
- IL-6 - IL-8 - IL-12 - TNF-α |
|
|
What are the important cytokines secreted by all T cells?
|
- IL-2
- IL-3 |
|
|
What are the important cytokines secreted by Th1 cells?
|
- IFN-γ
|
|
|
What are the important cytokines secreted by Th2 cells?
|
- IL-4
- IL-5 - IL-6 - IL-10 |
|
|
What are the important cytokines secreted by B cells?
|
IL-12
|
|
|
What are the important cytokines secreted by Regulatory T cells?
|
IL-10
|
|
|
How can you remember the functions of the first six interleukins?
|
Hot T-Bone stEAK:
- IL-1: fever (hot) - IL-2: stimulates T cells - IL-3: stimulates BONE marrow - IL-4: stimulates IgE production - IL-5: stimulates IgA production - IL-6: stimulates aKute phase protein production |
|
|
Which cytokines are endogenous pyrogens (causing a fever)? Source?
|
Macrophages:
- IL-1 - IL-6 |
|
|
What are the functions of IL-1? Source?
|
Macrophage:
- Endogenous pyrogen → causes fever - Osteoclast-activating factor - Causes acute inflammation - Activates endothelium to express adhesion molecules - Induces chemokine secretion to recruit leukocytes (Hot T-Bone stEAK: - IL-1 = fever (hot) |
|
|
What are the functions of IL-2? Source?
|
All T cells:
- Stimulates growth of helper, cytotoxic, and regulatory T cells (Hot T-Bone stEAK: - IL-2 stimulates T cells) |
|
|
What are the functions of IL-3? Source?
|
All T cells:
- Supports the growth and differentiation of BONE marrow stem cells - Functions like GM-CSF (Hot T-Bone stEAK: - IL-3 stimulates BONE marrow) |
|
|
What cytokine has a similar function as GM-CSF? Effect?
|
IL-3: Supports the growth and differentiation of BONE marrow stem cells
|
|
|
What are the functions of IL-4? Source?
|
From Th2 cells:
- Induces differentiation into Th2 cells - Promotes growth of B cells - Enhances class switching to IgE and IgG (Hot T-Bone stEAK: - IL-4 stimulates IgE production) |
|
|
What are the functions of IL-5? Source?
|
From Th2 cells:
- Promotes differentiation of B cells - Enhances class switching to IgA - Stimulates the growth and differentiation of eosinophils (Hot T-Bone stEAK: - IL-5 stimulates IgA production) |
|
|
What are the functions of IL-6? Source?
|
Secreted by macrophages and Th2 cells
- Endogenous pyrogen → fever - Stimulates production of acute-phase reactants (Hot T-Bone stEAK: - IL-6 stimulates aKute-phase protein production) |
|
|
What are the functions of IL-8? Source?
|
Secreted by macrophages:
- Major chemotactic for neutrophils "Clean up on AISLE 8" - neutrophils are recruited by IL-8 to CLEAR infections |
|
|
What are the functions of IL-10? Source?
|
From Th2 cells and Regulatory T cells
- Modulates inflammatory response - Inhibits actions of activated T cells and Th1 |
|
|
What are the functions of IL-12? Source?
|
Secreted by macrophages and B cells
- Induces differentiation of T cells into Th1 cells - Activates NK cells |
|
|
What are the functions of TNF-α? Source?
|
Secreted by macrophages
- Mediates septic shock - Activates endothelium - Causes leukocyte recruitment and vascular leak |
|
|
What are the functions of IFN-γ? Source?
|
From Th1 cells:
- Has antiviral and anti-tumor properties - Activates NK cells to kill virus infected cells - Increases MHC expression and antigen presentation in all cells |
|
|
Which cytokines activate NK cells?
|
- IL-12
- IFN-γ |
|
|
Which cytokine mediates septic shock?
|
TNF-α
|
|
|
Which cytokine is chemotactic for neutrophils?
|
IL-8 (clean up on aisle 8 by neutrophils)
|
|
|
Which cytokine increases MHC expression and antigen presentation in all cells?
|
IFN-γ
|
|
|
Which cytokine enhances class switching to IgE?
|
IL-4
|
|
|
Which cytokine enhances class switching to IgG?
|
IL-4
|
|
|
Which cytokine enhances class switching to IgA?
|
IL-5
|
|
|
Which cytokine stimulates the growth and differentiation of eosinophils?
|
IL-5
|
|
|
Which cytokine has a similar action to IL-10? How?
|
TGF-β and IL-10 both are involved in inhibiting inflammation
|
|
|
What molecules are part of the innate host defense against both RNA and DNA viruses?
|
Interferon α and β
|
|
|
What are Interferon α and β? Function?
|
- Glycoproteins synthesized by viral-infected cells that act locally on uninfected cells
- They prime the uninfected cells for viral defense (innate host defense against RNA and DNA viruses) |
|
|
What happens when a virus infects "primed" cells (by Interferon α and β)?
|
Viral dsRNA activates:
- RNAase L → degradation of viral / host mRNA - Protein kinase → inhibition of viral / host protein synthesis |
|
|
What is the ultimate effect of Interferon α and β on viral infected host cells?
|
Results in apoptosis, thereby interrupting viral amplification
|
|
|
What cell surface protein do all cells except mature RBCs have?
|
MHC 1
|
|
|
What cell surface protein do all T cells express?
|
- TCR
- CD3 - CD28 |
|
|
What is the function of the TCR? What cells express this?
|
Binds antigen-MHC complex
- Cell surface protein on all T cells |
|
|
What is the function of the CD3? What cells express this?
|
Associated with TCR for signal transduction
- Cell surface protein on all T cells |
|
|
What is the function of the CD28? What cells express this?
|
Binds B7 on APC
- Cell surface protein on all T cells |
|
|
What cell surface proteins do Helper T cells express?
|
All T cells: TCR, CD3, CD28
Specific to Helper T cells: - CD4 - CD40 ligand |
|
|
What cell surface proteins do Cytotoxic T cells express?
|
All T cells: TCR, CD3, CD28
Specific to Cytotoxic T cells: - CD8 |
|
|
What cell surface proteins do B cells express?
|
- Ig (binds antigen)
- CD19 - CD20 - CD21 (reeceptor for EBV) - CD40 - MHC II - B7 |
|
|
What is the receptor for Ebstein Barr Virus?
|
You can drink Beer at the Bar when you're 21: B cells, Epstein-Barr virus (CD21)
|
|
|
What cell surface proteins do macrophages express?
|
- CD14
- CD40 - MHC II - B7 - Fc and C3b receptors |
|
|
What is the function of Fc and C3b receptors on macrophages?
|
Enhances phagocytosis
|
|
|
What cell surface proteins do NK cells express?
|
- CD 16 (binds Fc of IgG)
- CD 56 (unique for NK) |
|
|
What is the function of CD16? What is it a marker for?
|
- Binds Fc region of IgG
- Found on NK cells |
|
|
What is the term for when self-reactive T cells become non-reactive without a co-stimulatory molecule?
|
Anergy
|
|
|
How does T cell anergy compare to B cell anergy?
|
B cells also become anergic, but tolerance is less complete than in T cells
|
|
|
What causes anergy?
|
Self-reactive T cells become non-reactive without co-stimulatory molecule
|
|
|
What bugs have super-antigens?
|
- S. pyogenes
- S. aureus |
|
|
What is the mechanism of the superantigens from S. pyogenes and S. aureus?
|
- Cross-link the β region of the T-cell receptor to the MHC class II on APCs
- Can activate any T cell, leading to a MASSIVE RELEASE OF CYTOKINES |
|
|
What is the mechanism by which endotoxins / lipopolysaccharide (on G- bacteria) stimulate an immune response?
|
Directly stimulate macrophages by binding to endotoxin receptor CD14
(Th cells are not involved) |
|
|
What is the function of CD14? Source?
|
Endotoxin receptor found on Macrophages - binds to endotoxins / lipopolysaccharide on G- bacteria - direct stimulation
|
|
|
What are some mechanisms for antigenic variation?
|
- DNA rearrangement
- RNA segment reassortment (eg, influenza major shift) |
|
|
What are examples of bacteria with antigenic variation?
|
- Salmonella: 2 flagellar variants
- Borrelia: relapsing fever - Neisseria gonorrhoeae: pilus protein |
|
|
What are examples of viruses with antigenic variation?
|
Influenza
- Major = shift - Minor = drift |
|
|
What are examples of parasites with antigenic variation?
|
Trypanosomes
- Programmed rearrangement |
|
|
What are the means of acquiring passive vs active immunity?
|
- Passive: receiving preformed antibodies
- Active: exposure to foreign antigens |
|
|
What is the relative onset of passive vs active immunity?
|
- Passive: rapid
- Active: slow |
|
|
What is the relative duration of passive vs active immunity?
|
- Passive: short span of antibodies (half-life = 3 weeks)
- Active: long-lasting protection (memory) |
|
|
What are examples of passive immunity?
|
- IgA in breast milk
- Maternal IgG crossing placenta - Antitoxin - Humanized monoclonal antibody |
|
|
What are examples of active immunity?
|
- Natural infection
- Vaccines - Toxoid |
|
|
After exposure to what bugs do you need to be given preformed antibodies (passive immunity)?
|
- Tetanus toxin
- Botulinum toxin - HBV - Rabies virus "To Be Healed Rapidly" |
|
|
After exposure to what bugs can you combine passive and active immunizations?
|
- Hepatitis B (HBV)
- Rabies virus |
|
|
What immunoglobulin is passed in breast milk?
|
IgA
|
|
|
What immunoglobulin crosses the placenta?
|
IgG
|
|
|
What is the purpose of vaccinations?
|
Used to induce an active immune response (humoral and/or cellular) to specific pathogens
|
|
|
What are the types of vaccines?
|
- Live Attenuated Vaccine
- Inactivated or Killed Vaccine |
|
|
What happens to make a live attenuated vaccine? What response does it cause in the host?
|
- Microorganism loses its pathogenicity but retains capacity for transient growth within an inoculated host
- Mainly induces a CELLULAR response |
|
|
What happens to make an inactivated or killed vaccine? What response does it cause in the host?
|
- Pathogen is inactivated by heat or chemicals
- Maintaining epitope structure on surface antigens is important for immune response - Humoral immunity is induced |
|
|
What are the pros of a live attenuated vaccine?
|
Induces strong, often lifelong immunity
|
|
|
What are the cons of a live attenuated vaccine?
|
- May revert to virulent form
- Often contraindicated in pregnancy and immune deficiency |
|
|
What are the types of live attenuated vaccines?
|
- Measles
- Mumps - Rubella - Polio (Sabin) - Influenza (intanasal) - Varicella - Yellow fever |
|
|
What are the pros of an inactivated or killed vaccine?
|
Stable and safer than live vaccines
|
|
|
What are the cons of an inactivated or killed vaccine?
|
- Weaker immune response
- Booster shots usually required |
|
|
What are the types of inactivated or killed vaccines?
|
- Cholera
- Hepatitis A - Polio (Salk) - Influenza (injection) - Rabies |
|
|
What happens in a type I hypersensitivity reaction?
|
- Anaphylactic and atopic
- Free antigen cross-links IgE on pre-sensitized mast cells and basophils - Triggers immediate release of vasoactive amines that act at post-capillary venules |
