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Immunology - Block 2 - Part 3

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davidwurbel7's version from 2015-10-29 20:50

The Generation of Humoral Effector Mechanisms

Question Answer
The main function of these is to neutralize toxins and viruses, to opsonize bacteria -> IgG and C3b component of complement bind to pathogen to enhance phagocytosis and activation of the classical complement pathwayAntibodies
Generally, the responses of this antibody have no memory, no isotype switching and no somatic mutationsT-Independent Antibody
These antigens contain no peptides, stimulate predominately IgM, and create no memoryThymus-Independent Antigens
B-cell contact with TH cells requires MHC class II/ peptide presentation, CD40/CD40L binding and this costimulatory moleculesB7
TH cells requires MHC class II/ peptide presentation, CD40/CD40L binding and costimulatory molecules (B7) to contact with this cell typeB Cell
Stimulates B cell growth and increases isotype switching and IgE productionIL-4
Stimulates B cell differentiation and increases eosinophils and IgAIL-5
The B cell simultaneously recognizes a microbial antigen by the immunoglobulin [Ig] receptorSignal 1
The B cell simultaneously recognizes bound C3d by the CR2 receptor forSignal 2
Disorder in which the gene encoding the CD40 ligand is defectiveX-Linked Hyper-IgM Syndrome
Small molecules that are antigenic but incapable by themselves of inducing a specific immune response and therefore lack immunogenicityHaptens
Chemical coupling of a hapten to a large immunogenic protein, called a carrier protein producing a hapten-carrier conjugate. This conjugate then is able to produceImmune Response
Constant-region determinants that collectively define each heavy-chain class and subclass and each light-chain type and subtype within a speciesIsotype Immunoglobins
Multiple alleles exist for some isotype genes that encode subtle amino acid differencesAllotype Immunoglobins
The conformation of the amino acid sequences of the heavy- and light-chain variable regions specific for each antigenIdiotype Immunoglobins
Major antibody produced after IgMIgG
Exists in four subisotypesIgG
Activates complement, opsonizes, and mediates Antibody-Dependent Cellular Cytotoxicity (ADCC)IgG
Actively transported across the placentaIgG
No known antibody function. Found on the surface of many B lymphocytes (required signal for mature B cells). Present in small amounts in serumIgD
Binds to mast cells and basophils. Mediates allergic type I immediate hypersensitivity reactions. Protects against parasites (helminths)IgE
Binds to Fcε receptors on mast cells and basophilIgE
Main immunoglobulin found in secretions. Most is produced in the submucosa. Is a dimer with a J chain. Inhibits binding of bacteria and viruses to mucosal surfaces. Important component in breast milkIgA
Immunoglobin that can activate the alternative complement pathwayIgA
Immunoglobin that can activate the classical complement pathway better than IgGIgM
Immunoglobin that can activate the classical complement pathway but not quite as well as IgMIgG
Main Ig produced early in the primary response. Plasma valence = 10 -> 10 identical epitopes can be simultaneously bound. Functions in trapping free antigenIgM
Affinity (binding strength) may be low Avidity (multipoint binding) highest of all isotypesIgM
Most effective isotype at activating complement. Is not an opsoninIgM
Does not mediate ADCC (antibody-dependent cell mediated cytotoxicity)IgM
Found in secretions such as colostrum, saliva, tears, and respiratory, intestinal, and genital tract secretionsIgA
IgA is produced by plasma cells in the lamina propria of mucosal tissue and binds to thisPoly-Ig Receptor
The IgA-Poly-Ig Receptor Complex is transported across the epithelial cell, and the bound IgA is released into the lumen by proteolytic cleavageTranscytosis
The process of transport across the cell, from the basolateral to the luminal surface in this caseTranscytosis
Prevention of the binding of microbes to cells and thus block the ability of the microbes to infect host cellsNeutralization
Antigen bound IgE bind to this high-affinity receptor on mast cell which induce the release of histamines and other cytokinesFcεRI
Receptor with high affinity for IgG. Found in macrophages, neutrophils and eosinophils. Activates phagocytesFcγRI
Receptor with low affinity for IgG. Found in macrophages, neutrophils, eosinophils and platelets. Ineffective activation of phagocyrosis. Clears immune complexes.FcγRIIA
Receptor with low affinity for IgG. Found in B lymphocytes. Functions as feedback inhibition of B cellsFcγRIIB
Receptor with low affinity for IgE. Found in NK cells. Functions for antibody-dependent cellular cytotoxicity (ADCC)FcγRIIIA
Receptor with high affinity for monomeric IgE. Found in mast cells, basophils and eosinophils. Functions to activate mast cell and basophilsFcεRI
Antibodies of the IgG1 and IgG3 subclasses bind to infected cells and the Fc regions of the bound antibodies are recognized by this receptor on NK cellsFcγRIIIA
FcγRIIIA receptors on NK cells binding to IgG1 and IgG3 can lead to thisAntibody-Dependent Cellular Cytotoxicity (ADCC)
During ADCC, eosinophils release these in order to kill the target cellPerforins and Granzymes
During ADCC, neurophils release these in order to kill the target cellLytic Enzymes
During ADCC, NK cells release these in order to kill the target cellPerforins, Granzymes and TNF
During ADCC, macrophages release these in order to kill the target cellLytic Enzymes and TNF
Receptor with low affinity for IgA. Found in monocytes, macrophages, neutrophils, eosinophils. Function: Phagocytosis and induction of microbe killingFcαRI
Generally equal to the number of antigen binding sitesValence
Strength with which a single epitope interacts with a single antigen binding site on an antibodyAffinity
Total strength of antigen-antibody binding when multiple epitopes on an antigen interact with multiple binding sites of an antibodyAvidity
B cell expresses only one allele for an antibody heavy chain and light chainAllelic Exclusion
Genes that encode enzymes that catalyze recombination of V, D, and J gene segmentsRAG-1 and RAG-2
Initiates processes that lead to somatic hypermutation, gene conversion and class switch recombinationActivation-Induced Deaminase (AID)
Enzyme that converts cytosine (cytidine) to uridine that leads to somatic hypermutationActivation-Induced Deaminase (AID)
An activated B cell that receives no signals begins to produceIgM
Under the influence of CD40 ligand (CD40L) and IFN-γ, the activated B cell switches to this classIgG1 and IgG3
Under the influence of CD40 ligand (CD40L) and IL-4 , the activated B cell switches to this classIgE and IgG4
Under the influence of CD40 ligand (CD40L), APRIL, BAFF and TGF-β, the activated B cell switches to this classIgA
Type 1 complement receptor (CR1) of phagocytes, recognize this resulting in ingestion and intracellular killing of the opsonized microbesC3b
C3b opsonizes microbes are recognized by this receptor of phagocytesType 1 Complement Receptor (CR1)
CR1 can also recognizes this opsonizing agent as wellC4b
Cytokines that cause smooth muscle contraction, histamine release from mast cells, and enhanced vascular permeability. They also mediate chemotaxis, inflammation, and generation of cytotoxic oxygen radicalsAnaphylatoxins
C3a, C4a and C5a components are referred to asAnaphylatoxins
The strongest anaphylatoxins isC5a
The second strongest anaphylatoxins isC3a
The least strong anaphylatoxins isC4a
Neutrophil attractant chemokineC5a
Large amounts of anaphylatoxins being produced by the body may result in this life-threatening conditionAnaphylaxis
Complement activation by the alternative pathway is activated by the binding of this to various activating surfacesC3b
Complement activation by the classical pathway is activated by the binding of this to antigen-antibody complexesC1
Complement activation by the lectin pathway is activated by the binding of this to microbesPlasma Lectin
C1 complex is composed ofC1qr2s2
C1qr2s2C1 Complex
C3 convertase for classical and lectin pathwayC4b2a
C3 convertase for the alternate pathwayC3bBb
C5 convertase for the classical and lectin pathwayC4b2aC3b
C5 convertase for the alternate pathwayC3bBbC3b
C5b, C6, C7, C8 and C9 form this complexMembrane Attack Complex (MAC)
Attaches and imbeds itself into the bacterial membraneC7
Forms a pore in the bacteria membrane resulting osmotic flux in the bacteria resulting in lysisC9
Protein that stabilizes C3bBb on the microbe surface membraneProperdin
This prevents C1qr2s2 from becoming activeC1 Inhibitor (C1 Inh)
Proteolytically cleaves C3b and C4b preventing the activity of C3 convertase in both the Classical and Alternative pathwaysFactor I
Causes disassociation of Alternative pathway C3 convertase subunitsFactor H
The first rearrangement in the variable region of the DNA is the joining of these two gene productsD-J Joining
The second rearrangement in the variable region of the DNA is the joining of this gene product with the product of the first rearrangementV-DJ Joining
Protease that cleaves Factor B into Bb and Ba when Factor B is bound to C3bFactor D
Protease that is the active protease of C3 and C5 convertaseFactor B
Results in profound susceptibility to infections, C3-deficient individuals develop autoimmune disorders, infections, or both. Infections tend to be recurrent and severe. Invasive infectionsDeficiency of C3
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Immunological Memory

Question Answer
Enables the immune system to respond more rapidly and effectively to pathogens that have been encountered previously, and prevents them from causing diseaseImmunological Memory
Memory is due to a small population of specialized cells formed during the adaptive immune response that persist in the absence of the original antigen that induced themMemory Cells
These cell have higher levels of cell-surface MHC class II and costimulatory B7.1 molecules on their surface so they initiate interactions with helper T cells at lower doses of antigenMemory B Cells
Expression of this subunit of the IL-7 receptor (CD127) identifies CD8+ effector T cells that generate robust memory responsesα Subunit (CD127)
These cells are required for the development of functional CD8+ memory T cellsCD4+ T Cells
This promotes cell survival of the memory cellsBCL-2
This memory cell expresses CCR7 chemokine receptor and reside in lymph nodesCentral Memory T Cells
This memory cell expresses CCR3 and CCR5 chemokine receptors and circulate throughout the bodyEffector Memory T Cells
Affinity of B cell receptors increases with each exposure to an antigenAffinity Maturation
These cells have higher levels of cell-surface MHC class II and costimulatory B7.1 molecules on their surface so they initiate interactions with helper T cells at lower doses of antigenMemory B Cells
T cells need activation but no cell division to become killers therefore, they can respond very fastCD8+ Memory T Cells
These cells require signals from contact with self-peptide-self MHC complexes and the cytokines IL-15 and IL-7 for survivalNaive T Cells
These cells require cytokines IL-15 and IL-7 for survivalMemory T Cells
These cells require signals from contact with self-peptide-self MHC complexes to proliferateMemory T Cells
These cells are required for the development of functional CD8+ memory T cellsCD4+ T Cells
When antigens have both epitopes that were “seen” before and new epitopes, the memory responses to the epitopes seen before will dominate, and there may be no response to the new epitopesOriginal Antigenic Sin
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