Immuno Flashcards
high renal oxygen demand is associated with
tubular O2 consumption used for solute reabsorption
sterile renal inflammation is induced by:
DAMPs
where do DAMPs come from in sterile inflammation
- parenchymal kidney cells
- generated during ECM degradation and remodeling
role of native C reactive protein (CRP)
binds DAMPs and activates complement classical pathway
how do classically activated M1 macrophages induce inflammation in the kidney
microbial TLR-ligands, interferon gamma, PAMPs, DAMPs activate the macrophages which then perpetuate the acute phase of inflammation in the kidney
how do alternatively activated M2 macrophages participate in the immune response in kidneys
induced by IL-4, IL-13 –> important in tissue repair and renal fibrosis
- also anti-inflammatory
what two cytokines control renal fibrosis from M2 macrophages
IL-10
TGF-B
type II hypersensitivity
- what antibodies
- antigen form
- mechanism
- IgG and IgM
- cell-bound
- complement activation and cell lysis
examples of type II hypersensitivity
patient with anti-glomerular basement membrane antibody-mediated GN
type III hypersensitivity
- what antibodies
- antigen form
- mechanism
- IgG and IgM
- solube
- complexes deposited in tissues, complement recruits neutrophils, enzymes from neutrophils damage the tissue
examples of type III hypersensitivity
- post-strep glomerulonephritis
- rheumatoid arthritis
- SLE
when are endothelial cells activated in immune response
- ischemia induced glomeruonephritis
- diabetes
- sepsis
when are dendritic cells and macrophages activated in immune response
DC: acute injury and infectino
M: most diseases
what 2 cytokines control tissue repair and renal fibrosis
IL-10
TGF-B
why do M2 macrophages stimulate pericytes during repair
pericytes lead to the differentiation of myofibroblasts which then leads to production of ECM
role of Tregs in AKI
secrete TGF-B and IL-10
anti-inflammatory
what are the targets for rejection in host versus graft transplants
histocompatibility antigens
how can you increase the chances of survival in xenografts
inserting human genes into the genome of hte donor animal
why is the father of a organ recipient a better fit for the transplant than the mother
the mother could have pregnancy-induced HLA sensitization, meaning they have pre-existing antibodies, which would lead to immediate hypersensitivity reactions
what are the three most important pairs of class II HLA for transplantation
HLA-DR
HLA-DP
HLA-DQ
when testing for class I HLA compatibility, what result would indicate identical HLA Ag
complement forms pores in the cells and dye accumulates in the cells
when testing for class I HLA compatibility, what result would indicate non-identical HLA Ag
no dye accumulation because complement did not form pores in the cells
host vs graft disease
recipient’s T cells attack the transplant
graft vs host disease
T cells in transplant attack recipients tissues
what happens if a second graft is performed from the same donor
the transplant is rejected more rapidly
what cells cause acute rejection
Th1 cells and CTLs
what cells cause chronic rejection
M2 macrophages and T cells
what cells cause hyperacute rejection
preexisting antibodies and complement
when and how does hyperacute rejection present
when: during surgery
how: thrombosis and occlusion of graft vessels
when and how does acute rejection present
when: weeks to months
how: inflammation and leukocyte infiltration of graft vessels
when and how does chronic rejection present
when: months to years
how: intimal thickening and fibrosis of graft vessels and graft atrophy
2 reasons for hyperacute graft rejection
- ABO incompatibility
- recipient has been sensitized to donor MHC by previous transplants/blood transfusions/pregnancy –> Abs bind to endothelial cells –> complement –> endothelium death
how does chronic graft rejection occur
indirect pathway
- macrophages infiltrate and smooth muscle proliferation occurs
- occlusion of blood vessels and ischemia of the organ occurs
3 non-immunological factors in chronic rejection
- ischemia-reperfusion damage
- recurrence of the disease that caused failure of own kidney
- effects of nephrotoxic drugs like cyclosporine A
does chronic rejection respond to immunosuppressive therapy
no
who does graft versus host disease occur in and why
immunocompromised patients
- their immune system is unable to reject the allogenic cells in the graft
where does acute GVHD occur and how does it appear clinically
where: epithelium in skin, liver, GI
how: rash, jaundice, diarrhea, GI hemorrhage
where does chronic GVHD occur and how does it appear clinically
where: affected organ
how: fibrosis and atrophy of organ, dysfunction of organ, obliteration of small airways
