Immuno Final Exam 2

Front 1

Paroxysmal Nocturnal Hemoglobinuria

Back 1

Lack of complement regulatory proteins (DAF and CD59) -> unchecked compliment and platelets and RBCs cannot repair damage --> hemolysis and thrombosis.

Front 2

CRP

Back 2

acute phase protein: binds phosphocholine on bacteria and can then be bound by complement. MBL can also bind bacteria and activate compliment

Front 3

TLR 2, TLR4

Back 3

binds yeast and LPS --> NFkB

Front 4

TLR 3

Back 4

Binds dsRNA --> IRF pathway (antiviral) --> IFN a and b

Front 5

Th17 cells

Back 5

-To protect us from extracellular pathogens and helminths, etc.
-Secrete IL-22, IL-6
-Activate NK, CD8, and macrophages to secret proinflammatory cytokines as well as to produce
-Important in RA and MS

Front 6

Abatacept

Back 6

CTLA-4 IG

Front 7

IL-2 or CD25 deficiency

Back 7

--> autoimmunity

Front 8

HSP-60

Back 8

A flag that T cells put up when they are activated by an intermediate avidity TCR:MHC interaction. T regs recognize flag and target T cell for suppression.

Front 9

IL-15

Back 9

Required for NK cell developmen

Front 10

CD16

Back 10

CD16 = FcgammaRIII and when NK cells are CD16 bright --> more cytotoxic than CD56 bright which is and adhesion molecule

Front 11

NK cells strategies to combat HIV

Back 11

ADCC, plus secretion of CCR5 to compete with HIV binding.

Front 12

MIPs

Back 12

chemokines produced by macrophages and DCs to attract DCs and NKs

Front 13

IP10

Back 13

attracts T-cells, secreted by macrophages

Front 14

p21, IL-12, FasL

Back 14

part of IRK pathway, causes cell arrest to stop viral spread, recruitment of CTL cells, and sensitization to death signal

Front 15

Critical features of IgA in mucosal immunity

Back 15

Resistant to proteases and cannot interact with complement which would --> inflammation

Front 16

Cytokines inducing isotype switching to IgA

Back 16

TGF beta, IL-2, IL-4, IL-5, IL-6 and IL-10 --> IgA-J

Front 17

J-chain on IgA

Back 17

B cells producing IgA in MALT express J chain while those in bone marrow do not. The J chain holds to IgA by constant ends together in dimer. The dimer in the lamina propria can form a complex with secretory component on the surface of mucosal epithelial cell. Then the complex and IgA are endocytosed and transported to lumenal side. There is a proteolytic cleavage of most of the component and the component and IgA are released into lumen.

Front 18

What is the single largest T-cell site in humans and which type of T cell resides there?

Back 18

Lamina propria, CD4

Front 19

What cytokines drive Th17 formation?

Back 19

TGF beta, IL-6, IL-23

Front 20

IELs: what are they? where are they? what do they do?

Back 20

Intraepithelial lymphocytes. CD8 t cells that reside between columnar epithelium. Show limited diversity and are 10% delta gamma. They are the first line of defense and secrete lots of TNF and IFN. they also modulate the epithelial cell renewal to maintain barrier.

Front 21

TH3 Cells

Back 21

T regs that secrete TGF beta

Front 22

TR1 cells

Back 22

T regs that secrete IL-10

Front 23

Oral tolerance and possible mechanisms

Back 23

Idea that oral administration of a protein can lead to tolerance to injection of same antigen in vaccine. CD8 T regs thought to be involved.
May induce anergy or clonal deletion of antigen specific T cells, or selective expansion of T regs

Front 24

CX3CR1

Back 24

Chemokine receptor that binds membrane bound chemokine. The receptor is expressed by DC circulating in lamina propria so they can protrude extensions into lumen. DCs also can receive peptide/Ag by M cell trancytosis.

Front 25

What's the difference between lymphoid follicles and peyer's patches

Back 25

peyer's patches lack and afferent lymphatic.

Front 26

IgA deficiency: How common is it? How does it present? What other problems can it cause?

Back 26

Most common Ig deficiency. Most individuals seem normal but discover difficiency when attempting to donate blood or upon undergoing anaphylactic shock with blood transfusion (b/c have IgE to IgA). Leads to higher risk for repiratory and GI tract infections. High incidence of autoimmune diseases (b/c keeps inflammatory response in check). Higher allergy incidence and higher celiac's incidence.

Front 27

Celiac's disease:
1) What is Ag
2) What is response
3) What is outcome?
4) Genetics

Back 27

1) Gluten (gliadin and glutenins)
2) Two processes don't know which comes first:
T cell mediated response of CD4 with MHC DQ 2 or 8. --> release of IFN-gamma
-and enterocytes become stressed and secrete IL-15 which activates IELs and there is increased leakiness and uptake of gluten to present to T-cells.
3) Inflammation, loss of villi with lymphocytic infiltrate and increased epithelial proliferation with crypt hyperplasia --> malabsorption.

Front 28

IBD
1) Includes what two diseases?
2) Features?
3) Loci involvement?

Back 28

1) Crohn's (distal small intestine and colon transmurally) and Ulcerative colitis (colon, superficially)
2) CD - Increase in CD4 cells secretion of IFN gamma, as well as cytokines stimulating Th1 and decrease in Tregs
Hummoral involvement: more IgG which is bad (CD: IgG2, UC: IgG1)
More inflammatory cytokines than regulatory
3) Nod2 mutations increases risk for CD 20-40%. Nod2 binding --> Paneth cell defensin production and inflammasome activation via APC.

Front 29

Infliximab

Back 29

anti -TNF therapy, used for many things possibly including IBD

Front 30

TIL

Back 30

Tumor Infiltrating lymphocytes. Include CTLs that recognize melanoma antigens. Problem is that CTLs could not produce IFN gamma, were essentially anergic (from lack of T cell priming). Likewise, Ab were found but only IgM

Front 31

TAMs
Growth and survival signals
Angiogenesis
Tissue invasion and metastasis
Mutations
Inhibition of T cell responses

Back 31

Tumor associated macrophages:
-FGF, EGF, PDGF, IL-6, TNF, PGE2
-VEGF, IL-1, IL-8, uPA, PGE2
-Chemokines, PGE2, MMPs, plasmin
-Superoxide, peroxynitrite
-IL-10, TFG-beta

Front 32

Method for T reg depletion

Back 32

IL-2 diptheria toxin conjugate, Anti-PD-1 (reversal of T cell exhaustion perhaps)

Front 33

Three strategies for induction of anti tumor immune responses

Back 33

1) Inject tumor cell with vector encoding immunostimulatory cytokines
2) Inject dendritic cells with viral vector, specific peptides, and tumor lysate
3) Subcutaneous injection of viral vector, peptide, and plasmid DNA

Front 34

Adjuvant effect

Back 34

Need to promote APC surveillance and uptake of antigen as well as recruit DC to injection site. Classical adjuvants = alum or Complete freunds adjuvant, emulsion of heat killed bacillus and oil and water. Molecular adjuvants = CD40L, and TLR ligands.