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EXAM 1: MLT 216
MLT 216: IMMUNOLOGY & IMMUNOHEMATOLOGY
| Question | Answer |
|---|---|
| True or False: Because antigen-antibody reactions are non-covalent, when sensitization occurs, the bond is reversible | true |
| What is the difference between affinity and avidity? | Affinity=initial strength of Ag-Ab bond Avidity=longevity and strength of that Ag-Ab bond |
| Describe why those who were exposed to cowpox confer immunity to smallpox | cross-reactivity; it can occur when antibodies are able to react to an antigen that has a similar makeup to the original antigen that it was produced in response to |
| Define the Prozone Phenomenon | this occurs when too much antibody is added to an assay, causing the antigens to bind without forming cross-links and producing a false negative result |
| What are some examples of precipitation assays and what are they | they assess whether or not a soluble antigen and a soluble antibody (both with multiple binding sites and similar concentration) will form an insoluble complex examples: nephelometry, turbidimetry, radial immunodiffusion, immunoelectrophoresis |
| What immunoassay principle involves antibody-embedded gels that-once an antigen is added-both will migrate towards each other and form a band precipitate? What is the purpose? | Immunoelectrophoreisis; characterizes the antibodies |
| What is the purpose of the complement fixation assay? | It assesses the presence of an antibody (IgG or IgM) based on its ability to form a Ag-Ab complex that complement can bind to, further preventing hemolysis when pre-sensitized RBCs are added to patient serum |
| A patient receives a non-reactive result from a complement fixation assay. What can we infer from this | The patient lacks an antibody (IgG or IgM) to form an Ag-Ab complex that complement can bind to. Therefore, when the pre-sensitized RBCs are added, antigen attaches to them, causing complement to bind them and cause hemolysis |
| Describe what would cause a reactive result for a complement fixation assay | After heating patient's serum of complement, known antigen and complement is added. The IgG or IgM should form a complex with the Ag, allowing complement to bind to the complex. when pre-sensitized RBCs are added, they fall to the bottom of the tube |
| What immunoassay utilizes a fluorescence labelled antibody to detect a specific antigen's presence? | Direct fluorescent immunoassay |
| What immunoassay utilizes fluorescence to identify the presence of antibodies of in patient serum? | Indirect fluorescent immunoassay |
| Describe the principle of the Chemiluminescent immunoassay | if an antigen is presence, a labelled antibody will bind to it and trigger a chemical reaction that produces light. the light is then read on a spectrophotometer |
| Why do we wash in an enzymatic immunoassay? | if the antigen is present, the enzyme-linked antibody will form a complex in it that will not be washed out. when the substrate is added, the color will change |
| What is the difference between the direct ELISA and indirect ELISA? | direct = present Ag causes labelled Ab to form complex, substrate added will change if antigen is present indirect= same, but unlabled Ab forms complex, then labelled Ab is added, the substrate |
| Which immunoassay's use of substrate color change is proportional to the quantity of antigen within a patient's serum? | Competitive ELISA |
| If a patient has an Absent/Low CH50 result alongside a normal AH50 result, what can we infer? | there is a deficiency within the classical pathway, or the patient has a condition (likely autoimmune) that causes complement consumption |
| What does MAC stand for? | membrane attack complex |
| If a patient has an Absent/Low AH50 result alongside a normal CH50 result, what can we infer? | there is a deficiency within the alternative pathway, or the patient is utilizing C5 inhibitor meds |
| If a patient has an Absent/Low CH50 result alongside a Absent/Low AH50 result, what can we infer? | there is a deficiency in C3, C5, and the MAC complement proteins (C6-9). or there is a significant amount of systemic complement consumption |
| What assay methods can be use to determine the reasoning for absent or low levels from a patient's complement efficiency testing (CH50/AH50) | radioimmunoassay and nephlometry |
| SLE causes deficiencies in (blank), while repetitive Neisseria infections causes deficiencies in (blank) | C2 or C4; C5-C9 |
| What complement regulator is responsible to preventing MAC complexes from forming and maintaining the terminal pathway? | vitronectin/S protein, |
| What causes HANE (Hereditary Angioneurotic edema)? | deficiency in C1 inhibitor, which causes spontaneous activation of C1 (classical pathway), resulting in swelling on the bod and GI tract |
| What is the purpose of DAF regulator? | controls C3 convertase in both pathways, causing disruption of C4b2a and C3bBb complexes |
| What are the main components that are monitored in complement regulation? Why does it need to be regulated | C1 for the classical pathway activation, MAC, C3 convertase in both paths, eliminate toxins that trigger anaphylactic symptoms complement proteins that go unchecked can cause asphyxia or tissue damage due to persistent inflammation |
| Define complement | a series of serum proteins that directly kill off foreign cells, coordinate inflammation and phagocytosis, and amp up antibody effects |
| Where is complement made, primarily speaking? | the liver |
| Which pathway is likely to be triggered by intravascular, bacterial invaders whose surface antigens interact with complement? | alternative |
| What is triggers the Lectin complement pathway? | the terminal sugars on bacterial cells |
| What triggers the Classical complement cascade? | IgM (or IgG) binding to a specific antigen |
| What is the Fc region of an antibody, and why is it integral to the classical complement cascade? | it is the non-specific heavy chain region that binds to host tissue. the more Fc regions in closer proximity, the more C1 can recognize the invader and fixation can occur |
| True or False: A deficiency in calcium will prevent the activation of complement in the alternative pathway | false; the classical pathway |
| What triggers the alternative pathway, and what complement proteins are not present? | recognition of multiple proteins on bacterial cell surfaces C1, C2, C4 |
| What triggers the Lectin pathway | MBL binds to the mannose sugar lining the cell wall, then activating MASP 1 and 2. |
| Describe the purpose of the MASPs | MASP 2 cleaves C4 and MASP 1 cleaves C2. The cleaving produces C4bC2a/C3 convertase, and the steps thereafter are the same as the classical pathway |
| Which antibody type is most abundant, fights off secondary infections, best at body temp for activation, but needs to be in close pairings for complement activation due to having less Fc points | IgG |
| What are some recognized limitations of vaccines? | 1) incorrect dosages can cause the disease youâre tryna prevent 2) side effects |
| What triggers the adaptive immunity | MHCs on cells presenting the antigen to a T-cell |
| Describe MHC II | genes coated on dendritic cells, macrophages, and B-cells that get antigens from extracellular pathogens and present them to CD4+ helper T-cells |
| Describe MHC I | genes coated on all nucleated cells that present an antigen from intercellular pathogens to CD8+ cytotoxic T-cells |
| Which T-cell does not form memory | Cytotoxic/Effector T-cells (CD8+) |
| Define a PAMP | Pathogen associated molecular patterns are recognized by Toll-like receptors, which aids in opsinizing pathogens |
| Define opsinization | the tagging of pathogens (after TLRs recognition of PAMPs) to mark them as non-self |
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