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;
82 Cards in this Set
- Front
- Back
What innate immune cells are the major defense against pyogenic bacteria?
|
Neutrophils
|
|
What innate immune cells combat bacteria, viruses, and protozoa that can live within cells?
|
Macrophages
|
|
How do innate immune cells recognize pathogens?
|
By PRRs which see PAMPs on the microbes.
|
|
What is an example of a PRR?
|
TLR
|
|
What is the function of TLRs?
|
To promote adherence and send danger signals that induce phagocytosis.
|
|
What system is used to attract phagocytic cells to microbes?
|
Complement
|
|
What does complement achieve?
|
Opsonization
|
|
What are the 3 cells that are major players in innate immunity?
|
-neutrophils
-macrophages -NK cells |
|
What are NK cells specialized for killing?
|
-Virally infected cells
-Tumor cells |
|
How do NK cells interact with other cells?
|
By 2-signal interactions
|
|
What are the 2 receptor interations that NK cells use to engage with viral or tumor cells?
|
-Cell surface recognition receptors
-MHC1/KIR interaction |
|
What is a KIR?
|
Killer inhibitory receptor
|
|
What happens when the KIR binds a cell with class I MHC?
|
The killer cell can't kill it because it is inhibited.
|
|
What happens when an NK cell's KIR does NOT bind an MHC I?
|
The NK cell can kill that cell that it is seeing because it lacks the inhibitory signal.
|
|
What is the other method of killing that NK cells utilize?
|
ADCC
|
|
What are the 3 components of adaptive immunity?
|
-Antibodies
-Tcells -Bcells |
|
What is the special feature that sets adaptive immunity apart?
|
Memory
|
|
What is an antigen?
|
A molecule that stimulates an immune response
|
|
What is an epitope?
|
The smallest part of an antigen that can evoke an immune response.
|
|
What are the sentinels of the immune system?
|
Dendritic cells
|
|
What are dendritic cells in the skin called?
|
Langerhan's cells
|
|
What does binding of antigen to immature dendritic cells cause?
|
Upregulation of Class II MHC
|
|
What happens after dendritic cell binding of antigen and upregulation of MHC II?
|
The complex migrates to the nearest lymph node to present the Ag/MHCII to Tcells.
|
|
What are the 2 components of adaptive immunity that are activated by antigen presentation in lymph nodes?
|
-Humoral immunity
-Cellular immunity |
|
Humoral immunity functions against:
|
Extracellular microbes
|
|
Cellular immunity functions against:
|
Intracellular microbes
|
|
How do antibodies kill pathogens?
|
By marking them for destruction by the innate immune system.
|
|
What does the Bcell receptor complex consist of?
|
-Membrane bound Ig
-Signal transduction molecules |
|
What are the 3 signal trnasduction molecules on the BCR complex?
|
-Igalpha
-Igbeta -CD21 |
|
How is BCR diversity generated?
|
By genetic recombinations.
|
|
How is TCR diversity generated?
|
By genetic rearrangements also
|
|
What are the 3 signal transduction molecules in the TCR complex?
|
CD3
zeta CD28 |
|
What cytokines promote leukocyte recruitment and acute inflammatory responses?
|
IL1 and TNF
|
|
What cytokine activates Tcells by binding to autologous receptors?
|
IL-2
|
|
What cytokine activates eosinophils?
|
IL5
|
|
What cytokine activates macrophages?
|
IFN-y
|
|
What cells are susceptible to EBV infection?
|
Bcells
|
|
What receptor is used by EBV to infect Bcells? What is the normal function of this receptor?
|
CD21 - the complement receptor (signal transduction molecule?)
|
|
What does the Bcell do once infected with EBV?
|
Presents chopped up peptides on Class II MHC to Thelper cells.
|
|
What is the Thelper response to antigen presentation by Bcells?
|
Secretion of cytokines which stimulate CTL proliferation to attack the virally infected bcells.
|
|
What is the characteristic Type I HSN reaction?
|
Allergy
|
|
What is the cause of allergy?
|
Overactivation of Th2 cells and IgE antibody production
|
|
What are genetically determined high levels of IgE called?
|
Atopy
|
|
What are the steps in Type I HSN?
|
-Allergen presented by DCs
-TH2 response secretes IL4,5,10 -IgE is secreted and coats mast cells -Subsequent exposure causes mast cell degranulation |
|
What are the 4 physiologic responses to mast cell release of primary and secondary mediators?
|
1. Smooth muscle spasm
2. Blood vessel dilation 3. Leukocyte infiltration 4. Mucus secretion |
|
What are the 2 classic examples of Type I HSN?
|
1. Bronchial asthma
2. Systemic anaphylaxis |
|
What is the cause of mucus secretion in bronchial asthma?
|
The late phase reaction caused by infiltrating neutrophils and eosinophils.
|
|
What are the 2 main treatments for bronchial asthma? What is each prescribed for?
|
1. Corticosteroids - to reduce inflammation
2. PDE inhibitors - to relax the bronchial smooth muscle |
|
What is the major initiating event of an acute allergic reaction?
|
Mast cell degranulation
|
|
What are the 2 major effects of Histamine?
|
-Smooth muscle contraction
-Vascular dilation |
|
What effect do proteases and prostaglandins and leukotrienes have?
|
Protease: tissue damage
Prostaglandin: vascular dilation Leukotrienes: smooth muscle contraction |
|
What is responsible for the late phase reaction of leukocyte recruitment?
|
Cytokines
|
|
What are the primary mediators in mast cell granules?
|
-Histamine
-Proteases -Chemotactic factors |
|
What are the secondary mediators in mast cells?
|
-Cytokines
-Eicosanoids |
|
What are the 2 products of arachidonic acid metabolism?
|
-Prostaglandins
-Leukotrienes |
|
What is the source of arachidonic acid?
|
Membrane phospholipid cleavage by Phospholipase A2
|
|
What additional 2ndary mediator is released from phospholipid metabolism by PLA2?
|
Platelet Activating Factor (PAF)
|
|
What is the rapidly developing systemic allergic reaction that can lead to shock and even death?
|
Systemic Anaphylaxis
|
|
What are common causes of systemic anaphylaxis?
|
Foods, drugs, insect venom
|
|
What are 2 clinical settings in which anaphylaxis could occur?
|
-Allergy shots
-Anesthesia |
|
Who discovered anaphylaxis and how?
|
Richet and Portier by studying portugese man of war in dogs.
|
|
What are the 2 main clinical manifestations of anaphylaxis?
|
1. Hypotension via vasodilation
2. Airway obstruction via laryngeal edema |
|
What is used to treat anaphylaxis?
|
Epinephrine
|
|
What is Type II hsn mediated by?
|
Antibodies against normal or altered cell surface antigens.
|
|
What are the 3 mechanisms by which antibody causes Type II hsn?
|
1. C' activation / opsonization
2. ADCC - KILLS the cell 3. Ab mediated cell DYSFUNCTION |
|
What is a Type II HSN disease in which Ab mediates cell dysfunction by STIMULATING it?
|
Graves disease
|
|
What is the antibody directed against in grave's disease?
|
The TSH receptor on thyroid epithelial cells
|
|
What is a Type II HSN disease in which Ab mediates cell dysfunction by INHIBITING it?
|
Myasthenia gravis
|
|
What is the antibody directed against in Myasthenia gravis?
|
The ACh receptor
|
|
So what is impaired in Myasthenia gravis?
|
Neuromuscular transmission
|
|
List 8 examples of Type II HSN disorders:
|
1. Grave's disease
2. Myasthenia gravis 3. Goodpasture's 4. Bullous pemphigoid 5. Pernicious anemia 6. Vasculitides 7. Thrombotic phenomena 8. Acute rheumatic fever |
|
What is the Ab specificity in Goodpastures?
|
Type 4 collagen
|
|
What are the clinical features of goodpastures?
|
-Nephritis
-Lung hemorrhage |
|
What is the Ab specificity in Bullous pemphigoid?
|
Epidermal basement membrane proteins
|
|
What are the clinical features of Bullous pemphigoid?
|
Skin vesicles
|
|
What is the Ab specificity in Pernicious anemia?
|
Intrinsic factor (from parietal cells in the gut)
|
|
What are the clinical features of pernicious anemia?
|
Megaloblastic anemia
|
|
What is the Ab specificity in Vasculitides?
|
Neutrophil cytoplasmic antibodies
|
|
What is the Ab specificity in Thrombotic phenomena?
|
Antiphospholipid antibodies
|
|
What is the Ab specificity in Acute rheumatic fever?
|
Streptococcal antibody that crossreacts with the heart
|
|
What is the clinical feature of acute rheumatic fever?
|
Carditis
|
|
What is a predominant site of autoantibody deposition in Goodpasture's syndrome?
|
The glomerulus
|