Term
| What are the five classes of immunoglobulins? |
|
Definition
IgA, IgD, IgE, IgG, IgM
(MEGDA) |
|
|
Term
| Which immunoglobulin forms pentamers? |
|
Definition
|
|
Term
| Which immunoglobulin forms dimers? |
|
Definition
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|
Term
| What is the term for the modern process to synthesize monoclonal antibodies (MAb)? |
|
Definition
|
|
Term
| List the steps of hybridoma technology |
|
Definition
1. Chemically fuse B cells (from mouse, immunized with antigen) and myeloma cells
2. Grow in drug-contained medium so only hybrid cells live
3. Select for antigen-specific hybridoma
4. Clone selected hybridoma cells |
|
|
Term
| What are the three possible outcomes of hybridoma technology? |
|
Definition
| Chimeric, humanized, or recombinant human |
|
|
Term
| Describe chimeric monoclonal antibodies |
|
Definition
| Mouse B cells with the constant region replaced with human |
|
|
Term
| Describe humanized monoclonal antibodies |
|
Definition
| The only parts of the antibodies that are "mouse" are the CDR loops, the rest is human |
|
|
Term
| Describe recombinant human monoclonal antibodies |
|
Definition
| Mouse monoclonal antibodies "turned" human using recombinant DNA technology |
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|
Term
Describe the structure of a B cell receptor. Where is the light chain? Where is the heavy chain? Where are the constant and variable regions?
(Diagram on back) |
|
Definition
|
|
Term
In a T-cell receptor, where are the variable regions? Where are the constant regions? What are the names of the two chains?
(Diagram on back) |
|
Definition
|
|
Term
|
Definition
| Soluble, very potent peptides and glycopeptides that stimulate (and/or inhibit) the survival, proliferation, differentiation, and/or function of different cell lines. |
|
|
Term
| Give two examples of cytokines |
|
Definition
| Interferons, Interleukins, etc. |
|
|
Term
| Give some examples of non-peptide mediators of inflammation. Where do they come from? |
|
Definition
Histamine, Leukotrienes, Prostaglandins, etc.
Derived from basophils, mast cells, and some other cell lines. |
|
|
Term
| List the five humoral amplification systems |
|
Definition
1. Complement
2. Kinins
3. Defensins
4. Coagulation
5. Inflammatory cytokines |
|
|
Term
| Define the complement system |
|
Definition
| The first line of defense, multi-protein system that is activated as a cascade to mediate inflammation, cytolysis, chemotaxis, and opsonization. |
|
|
Term
| What are the five major results of the complement system? |
|
Definition
1. Lysis of cells
2. Opsonization
3. Peptide fragments that regulate immune response
4. Regulate certain biological activity (cell division, antigen presentation, chemotaxis)
5. Vasodilation |
|
|
Term
|
Definition
| The process by which a pathogen is marked for ingestion and destruction by a phagocyte |
|
|
Term
| What are the three different pathways for complement activation? |
|
Definition
1. Classical pathway
2. Alternative pathway
3. Mannose-binding lectin pathway |
|
|
Term
| List the key steps in the classical pathway of complement activation |
|
Definition
1. IgG/IgM/C-reactive protein and C1q bind
2. This causes bioactive peptides C4a, C3a, and C5a to activate in a cascade
3. C3b, the key protein, is activated
4. C3b attracts C5, C6, C7, etc to make a pore
5. The membrane attack complex is formed |
|
|
Term
| What three things can initiate the classical pathway for the complement system? |
|
Definition
| One IgM, two IgG, or C-reactive prtoein |
|
|
Term
| Define C-reactive protein |
|
Definition
| One of the acute phase proteins produced following bacterial infections. Can activate the complement cascade. |
|
|
Term
| What is significant about complement protein C5a? |
|
Definition
| It is a chemoattractant for PMNs |
|
|
Term
|
Definition
The membrane attack complex, the goal of the complement system
Formation of a transmembrane pore, leading to cell lysis |
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|
Term
| List key steps in the alternative pathway to activate the complement system |
|
Definition
1. C3b binds without antibody activation
2. C3b attracts C5, C6, C7, etc to make a pore
3. The membrane attack complex is formed |
|
|
Term
| In the alternative pathway to activate the complement system, what triggers protein C3b? |
|
Definition
| The microenvironment of the microbial surface, not antibodies |
|
|
Term
| List key steps in the Mannose-binding lectin pathway to activate the complement system |
|
Definition
1. Mannose-binding lectin binds to pathogen surface
(rest of steps same as classical)
2. This causes bioactive peptides C4a, C3a, and C5a to activate in a cascade
3. C3b, the key protein, is activated
4. C3b attracts C5, C6, C7, etc to make a pore
5. The membrane attack complex is formed |
|
|
Term
| C3b is an important complement protein in all 3 pathways, as it tags the bacteria for destruction. What is the role of C3a? |
|
Definition
|
|
Term
| List the three methods of complement activation in the order in which they act |
|
Definition
1. Alternative
2. Lectin
3. Classical |
|
|
Term
|
Definition
Another inflammation mediator system that is activated as a cascade
Active in inflammation and smooth muscle contraction |
|
|
Term
| What is the final product of the kinin cascade? |
|
Definition
|
|
Term
|
Definition
| 9 amino acid peptide that causes vasodilation, hypotension, pain, smooth muscle contraction, and activation of arachidonic acid metabolism |
|
|
Term
|
Definition
| Short, amphipathic, antimicrobial peptides, typically 35-40 amino acids in length
Can penetrate membranes and destroy integrity |
|
|
Term
| What are the two classes of defensins? |
|
Definition
|
|
Term
| Define alpha-defensins. Where are they expressed? |
|
Definition
| Defensins expressed mainly by neutrophils and Paneth cells in the small intestine |
|
|
Term
| Define beta-defensins. Where are they expressed? |
|
Definition
| Defensins expressed by a broad range of epithelial cells, particularly on the skin, respiratory tract, and urogenital tract. |
|
|
Term
| How is the coagulation system involved in the immune response? |
|
Definition
1. Walls off microorganisms, prevents spread
2. Prevents loss of blood/fluid
3. Platelets release cytokines and other substances that promote inflammation |
|
|
Term
| What are the effect of inflammatory cytokines? |
|
Definition
| The acute phase response: raises body temperature and activates hepatocytes |
|
|
Term
| What acute phase proteins do inflammatory cytokines induce? |
|
Definition
Mannose-binding lectin and Creactive
protein |
|
|
Term
| List three inflammatory cytokines |
|
Definition
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|
Term
| What are the effects of inflammatory cytokines (IL-1, IL-6, TNF-α) on the liver? |
|
Definition
| Liver will produce acute-phase proteins (C-reactive protein and mannose-binding lectin) |
|
|
Term
| What are the effects of inflammatory cytokines (IL-1, IL-6, TNF-α) on the bone marrow endothelium? |
|
Definition
|
|
Term
| What are the effects of inflammatory cytokines (IL-1, IL-6, TNF-α) on the hypothalamus? |
|
Definition
| Increased body temperature |
|
|
Term
| What are the effects of inflammatory cytokines (IL-1, IL-6, TNF-α) on the fat and muscle? |
|
Definition
| Protein and energy mobilization to generate increased body temperature |
|
|
Term
| Why is it helpful to increase body temperature during an infection? |
|
Definition
| Decreased viral and bacterial replication |
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