Immuno

Question 1

high renal oxygen demand is associated with

Answer 1

tubular O2 consumption used for solute reabsorption

Question 2

sterile renal inflammation is induced by:

Answer 2

DAMPs

Question 3

where do DAMPs come from in sterile inflammation

Answer 3

• parenchymal kidney cells

- generated during ECM degradation and remodeling

Question 4

role of native C reactive protein (CRP)

Answer 4

binds DAMPs and activates complement classical pathway

Question 5

how do classically activated M1 macrophages induce inflammation in the kidney

Answer 5

microbial TLR-ligands, interferon gamma, PAMPs, DAMPs activate the macrophages which then perpetuate the acute phase of inflammation in the kidney

Question 6

how do alternatively activated M2 macrophages participate in the immune response in kidneys

Answer 6

induced by IL-4, IL-13 –> important in tissue repair and renal fibrosis
- also anti-inflammatory

Question 7

what two cytokines control renal fibrosis from M2 macrophages

Answer 7

IL-10

TGF-B

Question 8

type II hypersensitivity

• what antibodies
• antigen form
• mechanism

Answer 8

• IgG and IgM
• cell-bound
• complement activation and cell lysis

Question 9

examples of type II hypersensitivity

Answer 9

patient with anti-glomerular basement membrane antibody-mediated GN

Question 10

type III hypersensitivity

• what antibodies
• antigen form
• mechanism

Answer 10

• IgG and IgM
• solube
• complexes deposited in tissues, complement recruits neutrophils, enzymes from neutrophils damage the tissue

Question 11

examples of type III hypersensitivity

Answer 11

• post-strep glomerulonephritis
• rheumatoid arthritis
• SLE

Question 12

when are endothelial cells activated in immune response

Answer 12

• ischemia induced glomeruonephritis
• diabetes
• sepsis

Question 13

when are dendritic cells and macrophages activated in immune response

Answer 13

DC: acute injury and infectino
M: most diseases

Question 14

what 2 cytokines control tissue repair and renal fibrosis

Answer 14

IL-10

TGF-B

Question 15

why do M2 macrophages stimulate pericytes during repair

Answer 15

pericytes lead to the differentiation of myofibroblasts which then leads to production of ECM

Question 16

role of Tregs in AKI

Answer 16

secrete TGF-B and IL-10

anti-inflammatory

Question 17

what are the targets for rejection in host versus graft transplants

Answer 17

histocompatibility antigens

Question 18

how can you increase the chances of survival in xenografts

Answer 18

inserting human genes into the genome of hte donor animal

Question 19

why is the father of a organ recipient a better fit for the transplant than the mother

Answer 19

the mother could have pregnancy-induced HLA sensitization, meaning they have pre-existing antibodies, which would lead to immediate hypersensitivity reactions

Question 20

what are the three most important pairs of class II HLA for transplantation

Answer 20

HLA-DR
HLA-DP
HLA-DQ

Question 21

when testing for class I HLA compatibility, what result would indicate identical HLA Ag

Answer 21

complement forms pores in the cells and dye accumulates in the cells

Question 22

when testing for class I HLA compatibility, what result would indicate non-identical HLA Ag

Answer 22

no dye accumulation because complement did not form pores in the cells

Question 23

host vs graft disease

Answer 23

recipient’s T cells attack the transplant

Question 24

graft vs host disease

Answer 24

T cells in transplant attack recipients tissues

Question 25

what happens if a second graft is performed from the same donor

Answer 25

the transplant is rejected more rapidly

Question 26

what cells cause acute rejection

Answer 26

Th1 cells and CTLs

Question 27

what cells cause chronic rejection

Answer 27

M2 macrophages and T cells

Question 28

what cells cause hyperacute rejection

Answer 28

preexisting antibodies and complement

Question 29

when and how does hyperacute rejection present

Answer 29

when: during surgery how: thrombosis and occlusion of graft vessels

Question 30

when and how does acute rejection present

Answer 30

when: weeks to months how: inflammation and leukocyte infiltration of graft vessels

Question 31

when and how does chronic rejection present

Answer 31

when: months to years how: intimal thickening and fibrosis of graft vessels and graft atrophy

Question 32

2 reasons for hyperacute graft rejection

Answer 32

1. ABO incompatibility 2. recipient has been sensitized to donor MHC by previous transplants/blood transfusions/pregnancy --> Abs bind to endothelial cells --> complement --> endothelium death

Question 33

how does chronic graft rejection occur

Answer 33

indirect pathway - macrophages infiltrate and smooth muscle proliferation occurs - occlusion of blood vessels and ischemia of the organ occurs

Question 34

3 non-immunological factors in chronic rejection

Answer 34

1. ischemia-reperfusion damage 2. recurrence of the disease that caused failure of own kidney 3. effects of nephrotoxic drugs like cyclosporine A

Question 35

does chronic rejection respond to immunosuppressive therapy

Answer 35

no

Question 36

who does graft versus host disease occur in and why

Answer 36

immunocompromised patients | - their immune system is unable to reject the allogenic cells in the graft

Question 37

where does acute GVHD occur and how does it appear clinically

Answer 37

where: epithelium in skin, liver, GI how: rash, jaundice, diarrhea, GI hemorrhage

Question 38

where does chronic GVHD occur and how does it appear clinically

Answer 38

where: affected organ how: fibrosis and atrophy of organ, dysfunction of organ, obliteration of small airways