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69 Cards in this Set

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  • Back
What are innate immunity and acquired immunity?
Innate-normal physiological state of host. Nonspecific defenses
Aquired-immune response
What are the general characteristics of the immune response?
Specificity,memory, diversity, and discriminates self from nonself.
Can you define antigen, antigenic determinate, epitope, and hapten?
Antigen-elicits and recognized by immune response
Antigenic determinate or Epitope-like a receptor the site on the surface of an antigen molecule to which an antibody attaches itself
immune response recognition site
Hapten-Cannot elicit immune response by itself. Requires a carrier to elicit immune response (the epitope off of the antibody)
What are the two branches of the immune response?What class of cell mediates both of these types of responses
Humoral immune response and cellular immune response. Both are mediated by lymphocytes
Which particular subset of this cell type are responsible for the immunity?
Humoral immune response has B cells and Cellular immune response has T cells (direct effectors, regulators)
Where do each of these types of lymphocyes develope?
B cells-bursa/bone marrow, become memory cells/become plasma cells
T cells- Thymus
Know the fuction and derivation of the following cell types: TH1, TH2, Tc, Ts, Tdth, NK, B, and Plasma cell.
TH1-Stimulate the cellular immunity
TH2-Stimulate the humoral immunity
Tc-(direct effectors)cytotoxic T cells -CD8 positive. Recognize antigen in context of MHC Class 1.
Ts-(Regulaors)CD8 positive, recognize antigen in context of MHC Class 1. Suppress other cells.
Tdth-CD4 positive, recognize antigen in context of MHC Class 11, stimulate other cells, DELAYED type hypersensitivity.
NK-(null cells)(direct effectors)Lack CD4 and CD8 may or may not be a T cell, Kill cells.
Plasma cell-from B cells secrete antibody
Know the fuction and derivation of the following cell types: MO, Mast, and basophil
MO-Derived from monocytes they phagocytose and destroy pathogens;some active B & T cells.
Mast-Derived from the bone marrow. stimulated to degranulate by direct injury, binding of IgE to receptors, or by activated complement.VIDEO-
Basophils-Phagocytic leukocyte w/ granules(histamine, heparin)
Know the basic structure of an immunoglobulin (Ig) monomer.
Four polypeptides:
-2 heavy chains (H) determine class and antigen binding site
-2 light chains (L) determine antigen binding site
Constant, Variable(only in specific), amd hinge region
Papain digest yield what two types of fragments
Fab region/fragment(F-fragment A-Antigen B-binding)-antigen binding
Fc region/fragment-complement, CHO, Constant, crystal, cell, carboxy terminus, class
How many peptide chains are required to make a monomer?
What determines the class of an immunoglobin (antibody)?
The type of heavy chain determines the immunoglobulin isotype (IgA, IgD, IgG, IgE, IgM, respectively).More specifically, an isotype is determined by the primary sequence of amino acids in the constant region of the heavy chain, which in turn determines the three-dimensional structure of the molecule.
What determines the fxn for an antibody?
antibody structure, which determines antibody function
Most common in blood stream (70%). Monomer, 4 subtypes in humans,Activity: opsonin, activates CCP, agglutinates, neutralizes toxins & viruses.
-Crosses placenta
-Secondary response
Petamer, J chain holds together.
10%of lg in blood. Large retained in vasulature.
Activity: aggulutinin & activator of CCP
-First lg made by B cell
-monomer - serum - J chains form dimers
-dimer - secreted = sIgA
-major lg produced
-Secretory component added by mucosa epithelium(basement membrane)
-Secreted across all mucosa (cover J chain + Domains more resistant against proteases)
-Activity: agglutination, neutralization (Which is good b/c this is what the first toxins meet), activation of ACP
-make more then any other - not in blood (saliva, tears, etc.)
Monomer-mostly bound on B Cells
-Fuction-unknown but appears to signal lg production.
Monomer, traces in serum
-bound to Mast cells and basophils
Activity: Ag binding causes clustering and degranulation (w/ Ca2+ influx)
How do we generate such a tremendous diversity of antibody specificities?
We generate such a tremendous diversity of antibody specificites by rearrangement of antibody gene segments, somatic mutations, and generation of different codons during antibody gene splicing.
What happens at the genetic level during B cell development to commit a cell to a particular L chain antigen binding site?
During B cell differentiation, a deletion (variable in length) occurs that joins one V gene segment wih one J segment-Combinatorial joining-when transcription occurs the C region is also transcribed.
What happens during RNA processing?
During RNA processing all introns and suplerfluous exons are removed and the strand is spliced together (V,J, and C regions are joined.
How does H chain formation differ?
The H (heavy) chain differs in that it has a D (diversity) region; so that a VDJ region is joined to a C region.
Does this process also occur with other genes?
What do we mean by "class switching"?
"Class switch" is a change in the class of antibody that is produced (IgG, IgM, IgE, IgA); this depends on the specific deletion/recombination event that takes place and the resulting C region (determined by local factors).
Is this accomplished at the DNA or the RNA level? When does a clone do this?
This is accomplished at the DNA level and a clone does this when a particular antigen is present.
What is the T cell receptor and what cells have one?
The T cell recepter (TCR) is a receptor composed of two parts, an alpha and a beta polypeptide chain, that respond to antigen fragments exposed on the surfaces of antigen presenting cells (MHCI or II).
How many subunits do they have?
Two, an alpha and a beta that are stabilized by disulfide bonds.
In what context can it recognize antigen?
It can recognize antigen when it is presented on an MCH (class I or II).
Differentiate between Class I and Class II MHC molecules; How many subunits do they have?
Class I MHC molecules are found on all nucleated cells, it consists of 2 subunits (a and B2), and it binds with antigen in the lumen of the ER and presents it on the membrane-presents a sample of what's inside the cell. Class II MHC is found on all antigen presenting cells (B, M0), consists of 2 subunits (a & B), and it complexes with Ii in the ER, transport to endosome, switches Ii for antigen, and presents atigen on membrane-presents sample of what is outside the cell.
Do they have variable regions?
??Yes, there are variable regions in the B chain.
What is the role of the CD4 and CD8 molecules on T cells in discriminating between TCR recognition of Class I and II molecules?
CD4 molecules on T cells recognize antigen presented only by the MHC class II molecule, while CD8 molecules on T cells recognize antigen presented only by MHC class I molecules.
What is the Ii protein?
The Ii protein is a prot that the MHC class II molecule complexes with in the lumen of the ER and allows for translocation of the complex to the endosome.
Which MHC class is most likely to display antigen from an intracellular parasite?
MHC class I is mosy likely to display antigen from an intracellular parasite (it presents what is inside the cell).
When a M0 phagocytoses a bacterial invader, what is the initial antigen presenting cell (APC)?
The initial APC is an MHC Class II molecule.
What role does the Class II Histocompatibility Antigen play in the presentation?
It presents the antigen on the surface of the cell to CD4 T cells.
To what type of cell is the antigen being presented?
MHC class to-CD4 T cells
How is the specificity of the TCR determined?
T cell receptor is a molecule found on the surface of T lymphocytes that is responsible for recognizing antigens bound to major histocompatibility complex (MHC) molecules. It is a heterodimer consisting of an alpha and beta chain.The variable domain of the TCR α-chain has three hypervariable or complimentarity determining regions (CDRs), while the variable region of the β-chain has four CDRs.Processes for TCR formation are similar to those described for B-cell antigen receptors, otherwise known as immunoglobulins. The TCR alpha chain is generated by VJ recombination while the beta chain is generated by V(D)J recombination (both involve a somewhat random joining of gene segments to generate the complete TCR chain). Similarly, generation of the TCR gamma chain involves VJ recombination while generation of the TCR delta chain occurs by V(D)J is the unique combination of the segments at this region, along with palindromic and random nucleotide additions, which accounts for the great diversity in specificity of the T cell receptor for processed antigen
Successful antigen presentation by a M0 causes it to secrete what chemical messenger? What is another name for this molecule?
Interlueken 1 (IL-1); another name for IL-1 is endogenous pyrogen
In response to these chemical signals, the T cell produces what chemical signals?
Interleuken 2 (IL-2) AKA lymphokine.
What are two responses to being stimulated by IL-2 second message?
Two response to being stimulated by IL-2 are cell growth and proliferation.
What are cytokines, lymphokines, and interleukens?
Cytokines are nonanitbody proteins, released by the cell in responce to inducing stimuli, that effect other cells. Lymphokines are biologically active glycoproteins (eg. IL-1) secreted by activated lymphocytes-transmits growth, differentiation, and behavioral signals to other cells. Interleukens are glycoproteins produced by M0s and T cells that regulates growth and differentiation (*lymphocytes)-promote cellular & humoral immune response.
What are superantigens?
Superantigens are bacterial proteins that stimulate the immune system much more extensively than do normal antigens.
How do superantigens cause disease?
Superantigens stimulate T cells to proliferate nonspecifically through simulataneous interaction with class II MHC proteins on antigen-presenting cells and variable regions on the B chain of the TCR complex.
B cells can also act as antigen presenting cells; what cells do they present to in initiating a humoral response?
B cells present antigen to TH2 cells.
What happens to B cells when they present the appropriate antigen in the appropriate context and are stimulated by interleukens by TH cells?
B-cells are in the Class II MHC. They take in antigens, digest them and then present them on their cell surface on MHCII receptors. It is then that the CD4 T-helper cells recognize the peptide. Unlike CD8, CD4 do not directly kill the cell target, but instead they respond in two distinct ways: 1. enlarge and divide thereby increasing the number of CD4 cells that can react to the antigen 2. secrete cytokins(IL-2) that either directly inhibit the pathogen that produced the antigen or recruit and stimulate other cells to join in the immune response.
What are T-independent antigens?
A T-independednt antigen is an antigen that triggers a B cell into immunoglobulin production without T cell cooperation.
How does the response to T-independent antigens differ from that to T-dependent antigens?
T-indepentant: does not need T-Cell. Epitope polymers (LPS)can cross-link IgM receptors on B-cell surface. Stimulates limited B-cell proliferation and differentiation into plasma cells NOT MEMORY CELLS.
In the cellular immune response, what happens when the Tc Cells are stimulated by IL-2 and by antigen presentation?
-Become memory cells or
-cytotoxic lymphocytes (CTLs)

CTLs bind to target cells by recognizing antigen in the Class I MHC which then release TNF, perforins, and granzymes which induce apoptosis.
Where does the IL-2 come from?
TH1 create large amts of IL-2 which then activate Tc cells (page 727)
In what context is the antigen presented?
Antigen in context of MHC Class I on cell surface
How do CTLs recognize target cells? When they recognize them, what do they do and how do they they do it (include perforins, granzymes, and fas)?
CTLs bind to target cells by recognizing antigen in the Class I MHC.

CTLs release TNF, Perforins,Granzymes (all for apoptosis).

CTL CD95L bind ro target cell CD95 (fas) which induces the apoptosis.The Fas ligand or FasL is a type II transmembrane protein that belongs to the tumor necrosis factor (TNF) family.

Aliases include Fas ligand, FasL, apoptosis antigen ligand 1, CD95 ligand. It functions as a homotrimer.

FasL trimerizes FasR which spans the membrane of the "target" cell. This trimerization usually leads to apoptosis, or cell death.
What about NK cells? How do they recognize their target cells and kill them?
Activated by IFN or IL-2 and recognize Fc.
Attack antibody coated cells in context of Class I (ie with the antigen) or attack cells lacking MHC Class I antigen.

Induces lysosome and granules to target. Release perforins and Nitrogen species.
What occurs in each of these correlateds of the Clonal Selection Theory (the antigen selects the appropriate, precomitted clone): Clonal Amplification
Clonal amplification-specific cells are stimulated by Ag to reproduce and form B-cell clone whose cells contain the same info. (memory and specificity)
What occurs in each of these correlateds of the Clonal Selection Theory: Clonal Anergy
Context of presentation turns cell off.
What occurs in each of these correlateds of the Clonal Selection Theory: clonal Deletion
Destruction of self-reacting lymphocytes.

Neg. T cell selection in thymus-Removes cells from the thymus that:
-TCR that do not allow interaction w/MHC
-TCR bind "self antigen"

Positive T cell selection in thymus:
-TCR that allow interaction w/MHC clones multiply
What occurs in each of these correlateds of the Clonal Selection Theory: Clonal Suppression?
Ts cells control Th cells preventing response.
How do the latter three provide for immune tolerance?
Bodies ability to produce antibodies against nonself antigens while not producing antibodies against (tolerating) self-antigens.
What occurs when immune tolerance fails?
Failure creates auto-immunity and president Bush to be fired.
How do clonal amplification and class swithching lead to the anamnestic response?
anammnestic response=one that doesn't forget. It is the secondary response to the same antigen.

Clonal amplification-specific cells are stimulated by Ag to reproduce and form B-cell clone whose cells contain the same info. (memory and specificity)
Class switching-B-cells become memory or plasma cells
What are five characteristics of the secondary (anamnestic) response?
faster, greater, IgG, longer, more specific.
What are the four routes of acquisition of immunity? And give an example of each.
Activethat individuals immune system confers immunity.(ex. get a disease)
Passive-a different individuals immune system confers immunity.(snake bit serum made from horse)
Natural-immunity arises from a natural encounter with antigen (chicken pox)
Artifical-immunity arises from an artifical encounter with antigen (flu shot).
What types of hypersensitivities are represented by the following: Shock from a bee sting, shock from penicillin, hay fever, asthma, food allergies, hemolytic disease of the newborn, transfusion rxns(immediate), glomerular nephritis, farmers lung, poison ivy, and tuberculin test?
Type 1 anaphylactic, Type 1 anaphylactic, Type 1 atopic-upper resp. tract, Type 1 atopic lower resp. tract, Type 1 atopic-digestive tract, Type II Cytotoxic, Type II cytotoxic, Type III Immune complex, Type III Immune complex, Type IV cell-mediated or delayed,Type IV cell-mediated or delayed
What are the humoral and cellular mediators of type 1 (Anaphylactic/Atopic) Hypersensitivities?
IgE mediated. Primary exposure to allergen. IgE binds to mast cells and basophils. Binding by Fc portion of IgE. With second exposure to allergen: allergen + bound IgE = degranulation: Histamine, serotnin, SRS-A, Heparin, prostaglandins, ECF-A, etc.
Mediators: vasodilation, increased vascular permeability, smooth m. contractions(surrounds airways, smaller lumens), mucous secretion.
What are the effects of histamine, SRS-A, serotonin, and ECF-A?
vasodilation, increased vascular permeability, smooth m. contractions, mucous secretion.
What is the difference between anaphylactic and atopic?
Anaphylactic is a systemic reaction and atopic is localized reactions.
What is the humoral mediator of Type II (cytotoxic)Hypersensitivities?
IgG or IgM mediated
How does the deposition of the antibody in Type II differ from Type III? Where is the antigen?In what context is the antigen presented?
IgG & IgM, but in type III it is a soluble Ag +Ig. Complex absorbs to or ppts on cell surface. In type II antibodies bind cell surface.
Type II activates complement and lysis the cell and type III activated compliment and causes inflamation.Antigen in context of MHC Class I on cell surface
Where does the antigen-antibody complex form in Type III (Immune Complex Reaction) Hypersensitivities? and how does it cause damage?
Complex absorbs or pecipitates on cell surface. This then activates complex which causes inflamation which can cause damage to blood vessels, skin, etc.

In type 3 hypersensitivity, soluble immune complexes (aggregations of antigens and IgG and IgM antibodies) form in the blood and are deposited in various tissues (typically the skin, kidney and joints) where they may trigger an immune response according to the classical pathway of complement activation (see above). The reaction takes hours to days to develop.
How does Type IV (cell mediated) Hypersensitivity differ from all the other hypersensitivies? What type of cells predominate in the response?
Type IV is a cell-mediated or delayed which peaks after 2 days. Its a T-cell mediated response with MO moving to Ag site and presents Ag on cell surface. Responder is the Tdth which releases lymphokines for more lymphoctes, MO and basophils