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70 Cards in this Set
- Front
- Back
Host defense mechanisms
|
-natural barriers
-innate immunity -acquired immunity |
|
Natural barriers
-types |
-physical/anatomical
-absence of virus receptor -intracellular barriers that block replication |
|
Best natural barrier
|
-skin
|
|
Innate immunity
-types |
-RNAi
-Interferons/inflammatory cytokines -Phagocytic cells -NK cells |
|
Acquired Immunity
-types |
-TH1 immune response (CTLs)
-TH2 immune response (antibody) |
|
Good news about innate and adaptive immune responses
|
-redundancy
-integration |
|
Bad news about innate and adaptive immune responses
|
-immunity can be exploited by the pathogen to facilitate infection and disease
-immune activation can cause unintended consequences (neoplasia, autoimmunity, inflammation) |
|
Cells that are active early due to innate immunity
|
-IFN-Type 1
-NK cells |
|
Cells that are active later due to adaptive immunity
|
-Antibody (IgM)
-Neutralizing antibody (IgG) -CTLs |
|
Initial recognition of infection is due to:
|
-Pathogen-associated Molecular Patterns (PAMPs)
|
|
PAMPs
-types |
-dsRNA
-dsDNA in the cytoplasm -Viral proteins |
|
How are PAMPs recognized?
|
-Toll-like Receptors (TLRs) on the cell surface
-internal cellular receptors |
|
Danger signals of infection
|
-necrotic cell death
-inflammation |
|
Why do some vaccine adjuvants contain a product that induces some type of danger signal?
|
-to strengthen the vaccine potency
|
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How does RNAi provide host defense?
|
the host cell recognizes that there is something wrong in the genes coding for specific proteins so it destroys mRNA, not allowing it to code
|
|
RNAi
-process |
-recognition of dsRNA
-dsRNA cleaved by Dicer into small fragments -fragments incorporated into RNA-induced silencing complexes (RISCs) -use a single strand of fragmented RNA to find foreign RNA -degrades the target RNA |
|
Distances of Cytokine activity
|
-Autocrine (not measurable in body fluids)
-Paracrine (detected in pathological states) -Endocrine (measured in bodily fluids) |
|
Cytokine actions
|
-innate
-adaptive -inflammatory |
|
Interferons (IFN)
|
-produced by a virus infected cell to induces a virus-resistant state in surrounding cells (paracrine)
|
|
Type 1 Interferons
-produced by |
Multiple cell types:
-alpha -beta -kappa -delta |
|
Type 2 Interferons
-produced by |
-NK cells
-T cells |
|
Primary function of IFN on cell function
|
-upregulation of multiple cell pathways
|
|
Proteins upregulated by IFN
|
-PKR
-P56 -ADAR -2-5(A) synthetase |
|
Main protein upregulated by IFN
|
-PKR
|
|
PKR
-antiviral activities |
-activates other antiviral pathways
-induces apoptosis -inhibits protein synthesis |
|
P56
-antiviral activities |
-inhibition of cell division
|
|
ADAR
-antiviral activities |
-altered mRNA translation
|
|
2-5(A) synthetase
-antiviral properties |
-apoptosis
-mRNA degredation |
|
Protein Kinase R (PKR)
-function |
-recognizes dsRNA
-autophosphorylate and dimerizes dsRNA -eIF2-alpha binds and becomes phosphorylated -eIF2-alpha is turned off, terminated viral protein synthesis |
|
Methods viruses can use to subvert PKR
|
-inactive PKR
-dimerization inhibition -sequestration of dsRNA -active PKR inhibition |
|
How can viruses make PKR inactive
|
-downregulation
-inhibit activation -dsRNA analogs |
|
NK cell
-function |
-if a class-I MHC does not bind to the inhibitory receptor of the NK cell, the NK cell will become activated and kill the infected cell through apoptosis
|
|
Function of apoptotic blebs to NK cells
|
-increase the expression of activating ligands for NK cells
|
|
Adaptive immunity
-properties |
-recognition and activation by a specific foreign antigen
-effector function (production of cytokines, CTL, antibody) -memory |
|
Stages of adaptive immunity
|
-recognize antigens
-proliferation of B and T cells -implement effector functions -maturation of effector function -remove unused lymphocytes -memory |
|
2 roles of adaptive immunity
|
-virus specific antibodies prevent infection of cells
-cell-mediated immunity |
|
Cell Mediated Immunity
-transfer ability |
-cannot be transfered between animals
|
|
Humoral Immunity
-transfer ability -ex |
can be transferred between animals
-passive antibody in milk and transplacental -gamma globulin therapy |
|
When is it good to use gamma globulin therapy?
|
-if you don't have 2 weeks to wait for a vaccination to take effect
|
|
TH1 is what kind of immunity
|
Cell-Mediated Immunity
|
|
TH1 Cell-Mediated Immunity
-process |
-NK-cell causes virus infected cell to undergo apoptosis
-APC takes up the apoptotic bleb -Inflammatory cytokines are produced by the APC to alert of infection -The APC processes the antigen and presents it as MHC-II to a T-Cell receptor on TH1 (trimolecular complex) -Th1 will make IL-2 to drive the proliferation of more THC and make IFN through the paracrine response of IL-2 -IL-2 will also drive the proliferation of CTLs -a virus infected cell presents antigen as MHC-I to a CTL with a T-cell receptor, forming a trimolecular complex -the CTL kills the virus infected cell |
|
TH2 is what kind of immunity
|
Humoral Immunity
|
|
TH2 Humoral Immunity
-process |
-antibody on the resting B-cell is the receptor for antigen
-B-cell takes up antigen -antigen is presented by the B-cell as MHC-II to the TCR of TH2 (trimolecular complex) -TH2 cell produces B-cell cytokines -cytokines cause: B-cell proliferation, B-cell differentiation into plasma cells, and B-cell production of antibody |
|
MHC-I
-location |
-target cell
|
|
MHC-II
-location |
-presenting cells
|
|
Trimolecular complex
-components |
-MHC I/II
-Ag -TCR |
|
CD4
-purpose |
stabilize the trimolecular complex of Helper T-cells
|
|
CD8
-purpose |
stabilize the trimolecular complex of CTLs
|
|
What is the effect of a virus trying to downregulat MHC-I on the surface of the virus infected cell, in order to not be recognized by the CTLs?
|
-NK cells will recognize the missing MHC-1 and kill the cell
|
|
What is the end stage of CTL killing of a virus infected cell?
Why is this important? |
-the end stage is apoptosis
-it is important because it avoids an inflammatory response, and it provides apoptotic blebs with antigen to be recognized by APC |
|
3 ways that the CTL causes apoptosis
|
-granzymes
-perforin -FAS ligand |
|
What type of apoptotic signal is FAS ligand?
|
-extrinsic
|
|
How is apoptosis activated within the virus-infected cell?
|
caspase cascade activated by granzymes
|
|
2 regions of antibody
|
-Fab
-Fc |
|
Fab antibody region
-function |
-recognition
|
|
Fc antibody region
-Function |
-Function
|
|
How are the heavy and light chains of antibody held together?
|
-disulfide bond
|
|
Antibody type found in circulation
|
-IgG
|
|
Antibody type from naive B cells
|
-IgD
|
|
Antibody type responsible for allergies
|
-IgE
|
|
Antibody type that is found at mucosal surfaces
|
-IgA
|
|
Antibody type with high avidity
|
-IgM
|
|
Why is IgA important?
|
-most viruses enter the body through mucosal surfaces
|
|
Antibody
-actions |
-neutralize the virus infectivity of cells
-opsonize virus and virus-infected cells -complement-mediated lysis of enveloped viruses -antibody-dependent cell-mediated cytotoxicity |
|
Antibody
-bad effects |
-can facilitate infection with antibody-dependent enhancement of infection
|
|
Virus-neutralizing antibody
-function |
-bind to virus so that it cannot bind with the cell surface receptor
|
|
Opsonization antibody
-function |
-the ability to bind to the Fc receptor of a cell so that the virus gets taken up into a phagosome and degraded
|
|
Antibody Dependent Enhancement
-Function |
-virus uses the Fc receptor on a cell surface to facilitate infection
-the virus enters a cell endosome and replicates eventually resulting in infection |
|
Complement-Mediated membrane attack complex
-function |
remove the envelope from the virus making it unstable
|
|
Antibody-dependent cell-mediated cytotoxicity (ADCC)
-function |
-Fc receptors on the surface of NK cells recognize antibod bound to a virus infected cell
-When bound the NK cell releases granzymes and perforins, causing apoptosis |