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71 Cards in this Set

  • Front
  • Back
Immunoglobulin Cytokine Receptors
3 domains of 110 aa's, joined by disulfide bonds
ex - IL-1(fever), MCSF, C-Kit
Class 1 (hematopoietin) Cytokine Receptors
conserved CCCC motif and WSXWS
ex - IL-2->7, 9, 11->13, 15, GMSCF,GSCF,OSM,LIF,CNTF,GH,PRL
Class 2 (interferon) cytokine receptors
TNF Receptors
4 domains, C1C3C2
TNF-a,b, CD40, NGF, FAS
Chemokine Receptors
M-tropic - CCR5 (transmission, RANTES)
T-Tropic - CXCR4 (late infection)
CCR5(32) mutation - AIDS free disease.
Th1 Cells
Activated by IL-12 from macrophages, Stat-4 dependent.
Secrete- IL-2,IFN-gamma, TFN-b, GMSCF
Cell mediated immune responses (delayed type hypersensitivity)
Th2 Cells
Activated by IL-4 from activated t-cells, stat-6 dependent.
IL-4,5,10,13 - Humoral immune response (class switching), eosinophil and mast cell mediated immunity.
Bacterial Septic Shock
endotoxins stimulate overproduction of IL-1 and TNF-a
Fever, diarrhea, shock, clotting.
Bacterial toxic shock
sperantigens stimulate T-cells
macrophages produce high levels of IL-1 and TNF-a
Chagra's Disease
reduction of IL-2Ra by trypanosome cruzi.
Lymphoid and Myeloid Cancers
overproduction of IL-6
Contact-mediated activation of B cell
Bcell presents an Ag
TCR mediated inositol lipid hydrolysis - CD40L induced on Tcell - binds to CD40 of the Bcell, activates cytokine receptors.
B7/CD28 bind - induces MAP kinase -> cJUN (which binds cFos)
Cytoskeleton of Bcell rearranges (talin)-directional release of IL-4 - also needs IL-1 from macrophages.
Proliferation cytokines
Differentiation cytokines
IgA - IL-5 or TGF-b
IgG2 - INF-gamma
IgE - IL-4 + IL-13 or IL-5
IgM - IL-4 or IL-5 or IL-2
T-cell independent B cell activation Type 1
antigen binds a MITOGEN receptor
(TLR-4 for LPS)
mostly IgM
induction of polyclonal activation - Ig's secreted are not Ag specific.
No inositol lipid hydrolysis or calcium mobilization.
Tcell independent type 2 Ag's
crosslinking on membrane Ig
bacterial products.
IgM and IgG3 mostly produced.
Inositol lipid hydrolysis of PIP2 -> IP3 and DAG
Poised Tcell (CD8)
high p70(b) for IL-2R
low p55(a) for IL-2R
small amount of IL-2 produced, not enough to stimulate itself - requires IL-2 from CD4+
IL-2 increases p55(a) increased expression of IL-2R
on TC cell -> activation
Active Tcell (CD8)
granules - perforins, serine esterases(granzymes),toxins.
cytotoxic cytokines - TNFb (lymphotoxin-a), IFNgamma, and a little IL-2.
Lethal Hit
release of perforins, Ca-dependent polymerization of pores on membrane - toxins released from Tc can enter via pores, also osmotic lysis of cell - inflammatory response b/c release of lysozymes.
Also FasL/Fas triggered apoptosis of the cell - no inflammation.
CD40L deficiency
hyper IgM production, not germinal centers, no memory cells formed.
Perforin deficiency
genetic mutation - intace CTL, reduced killing of target cells by pore formation, increase in FasL/Fas mediated apoptosis.
Familial hemophagocytic lymphohistiocytosis.
Classical Complement
(Ab mediated)
1)binding of Ab to AG
2)C1 binds complex (c1q and c1r2s2)
3)C4 binds and cleaved by c1r2s2
4)C4b binds membrane.
5)C2 binds cleaved by C1r2s2.
6)C4b2a - C3 convertase.
7)C3 binds, cleaved
8)C3b binds membrane via thioester bonds.
9)C4b2a3b-C5 convertase
Ca and Mg dependent
Lectin Pathway
(MBP mediated)
1)MSAP-MBL binds membrane
2)C4 binds and cleaved by MSAP.
3)C2 binds and cleaved by MSAP.
4)C4b2a - C3 convertase.
5)C3 binds and cleaved.
6)C3b binds membrane
7)C4b2a3b - C5 convertase.
Ca and Mg dependent
Alternate Pathway
innate immune system
1)spontaneous cleavage of C3 in blood (low rate)
2)C3b may bind membrane
3)Factor B binds C3b
4)Factor D binds and cleaves B
5)C3bBb-C3 convertase.
6)C3 binds and cleaved.
7)C3b binds - C3bBb3b - C5 convertase.
Mg dependent.
Late Steps of Complement Activation
1)C5 binds and is cleaved.
2)C6 and 7 bind and complex inserted into cell membrane.
3)stable insertion of C8
4)15 C9's polymerize around the complex - MAC
complement inhibitor, prevents binding and activation of C1 - no C1r2s2 activity, can't cleave C2 or C4.
Deficiency=HANE, overproduction of C2b.
prevent assembly of C3 and C5 convertase, displace C2a from C4b (classical)
Alternate - only DAF and CR1 - displace Bb from C3b.
Factor I
serine protease in plasma, inhibits C3 convertase by cleaving C3b-iC3b
cofactors- MCP,CR1,FactorH
MAC inhibition
C59 - prevents C9 polymerization
serum protein S - prevents C5b-7 complex from being integrated into membrane.
neutrophil activation and mobilization, anaphalatoxin (a little)
mast cell degranulation
removal of immune complexes via RBC's
neutrophil activation
mast cell degranulation
Immune Complex Diseases
C1,4,2 deficiencies
MAC deficiency
predisposition to Neiserria
Deficiency in C3,D,I
pyogenic infections
Type 1 hypersensitivity
IgE mediated.
1)sensitization-1st exposure to Ag - Th2 cells activated (produce IL-4,13), Bcells produce specific IgE with bind FCER1 on mast cells.
2)tigger-repeat exposure, crosslinking of IgE on mast-degranulation.
Preformed Mediators
Histamine, Serotonin, chemotactic factors
Leukotrienes, prostaglandins, thromboxanes, PAF
Late-Phase Reactants
eosinophils, neutrophils - second wave of inflammation.
eopsinophil chemotactic factor (IL-3,4,5,13), eosinophilic cationic factor.
Type 2 hypersensitivity
activation of complement
NK-ADCC of Ab-coated cell
Ab may be bound to modified self Ag, attracts NK cells.
Type 2 hypersensitivity examples
Transfusion Reactions
Rhesus D (mother vs. fetus)
Autoimmune diseases - hemolytic anemia, drug-induced anemia, grave's disease, myasthenia gravis.
Type 3
immune complex mediated.
Local immune complex activates complement (deposited on walls of vessels) - blood vessel occlusion and inflammation - damage
Type 3 examples
SLE,RA, farmer's lung,arthus reaction(skin test, 6hrs), serum sickness.
Type 4
Delayed hypersensitivity.
Ag uptake, Th1 cells induced, recruitment of tcells,phagocytes, fluid, protein - visible lesion.
Skin test - 48-72 hrs.
Type 4 examples
contact dermatitis - poison ivy, metal ion reactions.
Insulin dependent diabetes mellitus.
Tuebrculin rxn.
Treat with steroids.
Molecular Mimicry examples
Type1 diabetes - CMV, rubella
Graves - yersinia enterocolitica
MS - EBV,herpes 6, milk-protein butyrophilin.
AS- cross rxn with HLAB27 and Klebsiella.
Rheumatic carditis-Strep
T and B cell deficiency
IL-2 and Il-7 receptor defects, also adenosine deaminase, purine nucleoside phosphorylase defects.
Di George
developmental thymic aplasia, no parathyroids, cardiac and facial abnormalities, tetany (low ca)
thymic grafts to treat.
Susceptible to pneumocystis carinii (fungal)
X linked agammaglobulinaemia
B cell defect (tyrosine kinase deficiency)
appears at 3-6 months.
HIV destruction of Tcells
Direct viral effect
Syncitium formation - cells with gp120 expressed bound by normal and infected CD4 cells - complex is removed.
Destruction by cytotoxic cells - NK cells, CTL, Macrophage.
Acute phase HIV
low or no Ab's produced,
high viral load,
ELISA test for Ab's and Western blot for Ab's - neither 100% in early phase.
Latent Phase HIV
gradual decrease in CD4,
Ab vs. HIV present (anti-gp41,120 and 24)
decreased viral load
CD4 around 400/microlitre
decrease in anti-gp24
increased viral load
CD4 below 200/microlitre
opportunistic infections take place.
Dendritic cells
langerhans-epidermis and mucosa
interdigitating-Tcell areas of secondary lymphoid tissues and thymic medulla
Circulating - aka veiled
Follicular-not APC, in Bcell rich follicles,facilitate Bcell activation in LN
chromosome 14
Ig heavy chain germ line
VDJ rearrangement
Chromosome 22,2
lambda and kappa light chains
one turn and two turn.
heptamer(palindromic) and AT rich nonamer conserved, random base pairs b/w.
One turn-12, two turn-23
Ig diversity
1)multiple genes for V region
2)multiple VJ and VDJ combinations
3)junctional flexibility in joining (CDR3).
4)Nucleotide additions - P-additions just add complement base pairs to hairpin. N-addition-adds random nucleotides to hairpin-TdT
5)Somatic hypermutations -affinity maturation
6)Combinatorial associations of H and L.
Pro Bcell maturation
triggers VDJ rearrangement of IgM heavy chain by kinase activity.
Pre B
Lose dependency on CKit and SCF for binding IL-7 growth factor.
IgM chain rearranged, SL produced, lambda5:VpreB. Expressed on surface with M heavy chain- interacts with Igalpha/beta and signals light chain rearrangement.
Chromosome 6
Class I - A,B,C
Class II-DP,DQ,DR,DM(like)
b/w DM and DQ - TAP1/2 and LMP
Class3-soluble factors, cytokines, complement(4,2,factorb)TNF.
Chromosome 17
H-2 - mouse
Class1- K,D,L
Class2- IA,IE,M
Class3-soluble factors.
MHC II stucture
heterodimer, alpha and beta chains.
Alpha1 and Beta1 are highly variable, 2's are conserved.
MHC I Structure
alpha chain and associated B2 microglobulin (not on same chromosome - 15(human),2(mouse)
B2MG bound to highly conserved alpha3
MHC polymorphism
variation not random-specific localization.
no hypermutation.
Polymorphism at the amino terminal domains (a1,a2 of MHC1,a1+b1 of MHC2)
Adhesion of Th to APC
Ag Recognition (Tcell activation)
TCR:MHC+Ag (low affinity-serial engagement)
Immunological synapse formation - CD2 and LFA-1 move and encircle TCR/MHC
Activation of Tcell
Tcell signaling TCR/CD3
TCR/CD4:MHC/Ag - juxtaposition of Lck and ITAMS of CD3
CD45:CD22-activation of tyrosine phosphatase at bottom of CD45- dephosphorylates Fyn+Lck (now active)-
phosphorylate ITAMS
phosphorylated ITAM of zeta binds ZAP-70 to zeta - activated.
ZAP-70 and Fyn phospharylate PLC-gamma1
cleaves PIP2-> IP3 and DAG
IP3 binds Ca channels and releases intracellular ca stores. Icreased [ca] binds PKC to pm, activated by DAG. Also Ca/calmodulin - activates calcineurin phosphatase - dephos. of NF-ATc-PO4 ->NF-AT, binds enhancer region on gene.
phos. inhibition factor, release of NF-KB, binds to another enhancer region on gene.
also activates protooncogene cFOS, interacts with cJUN, forms AP1 and NF dimer on IL-2 enhancer region