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70 Cards in this Set
- Front
- Back
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Immunological Memory |
enhanced immune response demonstrated on subsequent exposure to pathogen |
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primary adaptive immune response |
clears first exposure and establishes protective immunity and immunological memory |
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protective immunity |
residual T cells that circulate for about 3 weeks and antibody which will fall to a low level. low level antibody titer achieved by plasma cells. |
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function of protective immunity |
prevents reinfection from family, co-workers, roommates, spouse etc. |
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location and development of plasma cells |
located in the bone marrow, must be given BAFF IL-6 survival signal by bone marrow stromal cells. |
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advantages of memory B cells |
memory B cells outnumber naive B cells due to clonal proliferation. Memory B cells are readily activated |
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why are memory B cells readily activated |
They respond to lower concentration of antigen due to class switching to a more effective isotype and stronger cognate interaction with T cells. Continues somatic hypermutation/affinity maturation during secondary immune response with more effective memory B cells and stronger BCR affinity. |
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advantages of memory T cells |
Ag specific memory T cells outnumber naive T cells due to clonal proliferation. Circulate peripheral tissue to activate at infection. Doesnt' need B7(Tc CD28) costimulation |
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how do memory cells survive |
long lived quiescent cells that die but are replenished. survival requires stimulation of IL-7 and IL-15 produced by stromal cells in bone marrow. |
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memory cells small pox evidence |
small pox vaccine was terminated in 1972 and eradicated by 1979. vaccinated people maintain protection for years due to antibody production of long lived plasma cells and CD4/CD8 T cells specific for small pox. |
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Advantages and disadvantage of secondary adaptive immune response |
Advantage: only activates memory cells and suppresses naive cells to use metabolic resources more efficiently Disadvantage: bad strategy for mutable pathogens like influenza |
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how are naive B cells downregulated |
Inhibited via Fc[gamma]RIIB1 ligation to IgG Fc remaining from old infection or from long lived plasma cells |
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how does RhoGam work |
IgG-antiD coat Rh+ fetal cells entering mothers circulation. IgG ligates with Fc[gamma]RIIB1 on naive B cells and mother doesn't produce anti-D against fetal blood |
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pattern of original antigenic sin |
1st: primary IR to epitopes ABCD leads to full illness develops memory 2nd: mild infection due to immunologic memory ABC but not E (suppressed) 3rd: mild infection due to immunologic memory AB but not EF (suppressed) 4th: more severe infection due to only A for immunologic memory but EFG (suppressed) 5th: primary IR to epitopes EFGH leads to full illness develops memory |
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three types of barriers of infection |
mechanical, chemical, and microbiological |
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mechanical barrier |
epithelial lining with tight junctions. filtering of respiratory tract via turbinates mucus/cilia. |
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chemical barrier |
lysozyme with antibacterial action tears and saliva acid pH in the stomach, vagina, skin surfactant coat pathogen surface enhance phagocytosis |
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microbiological barrier |
commensal microbes create competitive environment that secrete antibacterial protiens |
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what is compliment system |
plasma proteins c1-c9 activated by alternative, lectin, and opsonization pathway |
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pathogen protease function |
spread infection, damage host tissue, damage defenses
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function of protease inhibitors |
inhibit microbiological proteases alpha-2 macroglubulin uses a protease bait which when cleaved traps enzyme in thioester covalent bond. |
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what are defensins |
family of proteins of microbial peptides expressed at mucosal surface 35-40 aa long positive arginine amphipathic molecule penetrates and disrupts membrane |
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alpha vs beta defensins |
alpha are produced by neutrophils and paneth cells of the small intesting beta are produced by epithelial cells on the skin, GI tract, respiratory tract, and urogenital tract |
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unique genetics of defensins |
number of copies vary between individuals 2-14 for alpha and 2-12 for beta. Copy number influence how many are made. Old mechanism used by plants and animals |
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structure and function of pentraxins |
5 subunit molecule residing in blood lymph that bind to pathogen surface and target it for destruction |
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location and function of serum amyloid P (SAP) |
expressed by liver hepatocytes that bind carbohydrate LPS of pathogen. Fc[gamma] receptors trigger phagocytosis and activates compliment leading to lysis |
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structure and function of PTX3 |
similar to SAP at c terminus but longer N terminus. produced by inflammatory cells bind Fc receptors leading to phagocytosis. activates compliment leading to lysis |
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toxic oxygen derivatives: myeloperoxidase depedent |
myeloperoxidase granules convert hydrogen peroxide and a halide (Cl) to hypohalite. Hypohalite oxidizes and destroys microbe protein. |
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toxic oxygen derivatives: myeloperoxidase independent |
NADPH oxidase is activated in the plasma membrane. This enzyme oxidizes NADPH to produce superoxide and hydrogen ion. This reacts with superoxide dismutase to produce hydrogen peroxide. This forms superoxide, singlet oxygen, and hydroxyl radicals |
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toxic oxygen derivatives: nitric oxide |
nitric oxide synthase converts arginine+oxygen into citrulline and nitric oxide which is toxic. |
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non-oxidative microbial agents |
acid of phagosome defensins alpha and beta lysozymes acid hydrolase degredative enzymes lactoferrin and gelatinase bind iron and vitamin B12 to create nutrient competition |
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function of lysozymes |
active against peptidoglycan gram positive bacteria |
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Inflammation |
series of reactions by way of cells and molecules that are recruited to sites of tissue damage characterized by swelling, redness, pain, and heat |
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Inflammation pathway |
vasodialation increases blood flow endothelium produce adhesion molecules release chemokines CXCL8 for neutrophils increase vascular permeability for diapedesis and moves plasma in endotherlium produces platelet activating factor PAF creates clots to stop infection from spreading |
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macrophage cytokines |
IL-1B, IL-6, IL-12, CXCL8 TNF[alpha] |
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advantage and disadvantage of TNF[alpha] |
advantage: in a local infection, increase of lymph flow delivers antigen to SLT for adaptive immune response disadvantage: systemic release leads to endotoxin shock |
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endotoxin shock |
complication of gram negative bacteria septicemia due to LPS stimulating macrophages of liver or spleen. characterized by TNF[alpha] release, drop in blood pressure, and disseminated of intravascular clotting |
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toxic shock syndrome |
super antigen can activate a large number of CD4 cells non-specifically. Interrupts the alpha chain of MHCII and beta chain of TCR as well as B7-CD28 ligation. T cell activation and proliferation leads to release of TNF[alpha], IL-2, and IFN[gamma] |
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superantigens |
molecules that are not processed by an APC. no binidng groove and bound non-specifically. These cause release of TNF[alpha] from Thelper cells. Reduction of t cell count leads to reduced efficiency of adaptive immune response |
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Fever causes |
macrophage inflammatory cytokines IL-1, IL-6, TNF[alpha]. reset thermal control in hypothalamus. vasoconstriction for heat conservation. alter metabolism of fat and muscle for heat. |
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Acute phase response |
acute phase proteins released from liver stimulated by macrophage release of IL-6. produced within 1-2 days |
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name the acute phase proteins (APP) |
C reactive protein, mannose binding lectin, fibrinogen, and serum amyloid A |
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APP: C reactive protein |
pentraxin with ligand of LPS. Opsonin by binding Fc[gamma]RI and Fc[gamma]RII for phagocytes activates classical pathway |
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APP: mannose binding lectin |
ligand mannose containing carbohydrate of pathogen Opsonin activates lectin pathway |
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APP: fibrinogen |
produced to support blood coagulation associated with inflammation |
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APP: serum amyloid A |
interacts with TLC and scavenge receptors of cells to release inflammatory cytokines which amplify inflammation initiated by pathogen |
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diseases associated with chronic inflammation |
MI, strokes, Alzheimer, cancer |
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how does chronic inflammation cause disease |
macrophages enter to remove plaque. macrophage inflammation may destabilize and rupture plaque causing blood vessel occlusion |
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how do statins work |
statins lower both LDL and CRP. CRP 3 ug/ml increased risk of MI by 3x |
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where are interferons produced |
virally infected cells and plasmacytoid dendritic cells |
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type I interferons |
IFN[gamma] activate TH1, CD8, NK cells
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type II interferons |
macrophage activation enhances phagocytic activity and increase synthesis of microbicidal agents. |
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detection of viral infection |
RNA is detected with RLR (RIG like receptor) |
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events to interferon response from RLR |
RLR detect RNA via helicase domain RLR binds to MAV via card domain RLR dimerizes causing signalling IRF3 (interferon response factor) activated IFN[beta] released causing IFN response |
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interferon response |
activation of NK cells that kills virally infected cells. increased expression of NK cell receptor ligands by VIC enhances NK cell identification |
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viral resistance to degrade RNA |
IFN [alpha/beta] bind to uninfected cell and induces expression of 2' 5' oligoadenylate synthetase polymerizes ATP via 2' 5' linkage adenine trinucleotide activates endoribonuclease to degrade the RNA |
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viral resistance to impair replication |
IFN [alpha/beta] bind to uninfected cell activates protein kinase R (PKR) PKR phosphorylates/inactivates eIF-2 (eukaryotic initiation factor) eIF-2 inhibits translation impairing protein synthesis to impair replication |
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therapy of IFN[alpha/beta] |
use against Hep B,C antiviral leukemia increases-NK cells MS-autoimmune regulation |
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structure and function of plasmacytoid dendritic cell. pDC |
aka interferon dendritic cell plasma cell morphology DC lymphocyte but lack a BCR or TCR located in the bone marrow but rare in blood accumulates in inflamed LN antiviral action via IFN release[alpha/beta] |
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receptor expression in pDC |
antigen BDCA-2 ILT-7 (immunoglublin like transcript 7) CXCR-3 chemokine produced by T cells used for migration into lymph node TLR-7 ssRNA detection TLR-9 unmethylated CpG rich DNA viruses |
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location and structure of NK cells |
natural killer cells lack TLR or BCR large granular lymphocytes originated in bone marrow, they recirculate between blood and tissues |
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receptors on NK cells |
CD56-adhesion Fc[gamma]RIII (CD16) NKG2D present in all NK cells random assortment of inhibitory/activating receptors |
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function of NK cell in uterus |
secrete growth factor to enlarge blood vessels in uterus to placenta and secrete non-inflammatory cytokines and prevent uterine tissue rejection |
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function of NK cells |
cytotoxic action against virally infected cells active macrophages lead to inflamamtion and more IFN[gamma] activating more macrophages |
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NK cell activation |
release of type 1 IFN stimulated by IFN[alpha/beta] by virally infected cells or pDC |
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how do NK cells distinguish healthy from virally infected cells |
activating receptor NKG2D ligates with MIC MIC A/B are stress induced stress high MIC cells are ligated to NKG2D and cytotoxic action takes place overridden by MHC I ligation |
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NK cell cytotoxicity |
apoptosis via perforin or granulysin TNF[alpha] FasL given by CD8 cells to commit that cell to apoptosis. Death signal |
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role of NK cells in cancer |
Cancer cells decrease MHC I and therefore stop expressing inhibitory receptor lower IR and high MIC ligates more NKG2D activator allowing for destruction |
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what is the role of antibody dependent cell mediated cytotoxicity ADCC |
Utilizes Fc[gamma]RIII (CD16) which ligates with IgG antigens |
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how does inflammation leads to macrophage activation |
macrophage releases CXCL8 NK chemokine NK cell-macrophage cognate pair IL-12 and IL-15 activates NK cell effector NK cell releases IFN[gamma] activates macrophages |
