Final Immuno

Question 1

• Most cases of AKI are caused by _

Answer 1

Sterile inflammation

Question 2

• CRPs have IgM subunits that bind DAMPs and activate

Answer 2

Classical compliment pathway

Question 3

• Classical compliment attracts immune cells
• Immune cells recognize DAMPs via _ receptors
• Immune cells do what

Answer 3

• Toll Like
• Initiate immune response and stimulate renal inflammation

Question 4

• What triggers the release of DAMPs

Answer 4

• Dying kidney cells
• ECM degradation and remodeling

Question 5

• PAMPs are _

Answer 5

• Pathogen derived

Question 6

• DAMPs are _ derived

Answer 6

• Cell/ECM

Question 7

• Th1 and Th2 cells are _ exclusive

Answer 7

• Mutually
• Increase in one causes a decrease in the other (and vice versa)

Question 8

• M1 macrophages are responsible for _

Answer 8

• AKI

Question 9

• M2 macrophages are responsible for _

Answer 9

• Damage repair

Question 10

• What induces the activation of M1 macrophages?
• What do they secrete that helps activate Th1 cells?

Answer 10

• IFN Gamma
• IL-12

Question 11

• When are M2 macrophages activated?
• What cytokines induce their activation?

Answer 11

• ~ 7 days
• IL-4, IL-13

Question 12

• What cytokine do M2 macrophages release for anti-inflammatory effects

Answer 12

• IL-10

Question 13

• What cytokine do M2 macrophages release that serves as a growth factor for fibroblast and stimulates wound repair/fibrosis

Answer 13

• TGF Beta

Question 14

• By default, T cells differentiate into?
• What cytokine stimulates this?

Answer 14

• Th2
• IL-4

Question 15

• Which type of T cell is important for tissue inflammation?
• What do they secrete?

Answer 15

• Th17
• IL-17
• CCL-20/MIP-3​

Question 16

• What does IL-17 do?
• What does CCL20/MIP-3?

Answer 16

• Tissue inflammation
• Recruits monocytes, Th1, Th17 cells

Question 17

• Which complement pathways are activated in AKI?

Answer 17

• Classical
• Alternative
• MBL

Question 18

• AKI is Types _ and _ Hypersensitivity

Answer 18

• II and III
• II=cell bound IgM and IgG bind cellular Ag, compliment activation and cell lysis
• III=Ag-Ab complex is deposited in tissues and initiates complement activation, inflammatory mediator activation, and recruitment of neutrophils

Question 19

• Host v. graft response is a _ immune response

Answer 19

• Adaptive

Question 20

• Direct allorecognition

Answer 20

• T cells from recipient recognized unprocessed allogenic MHC molecules on graft APCs

Question 21

• Indirect allorecognition

Answer 21

• T cells of donor recognize processed peptide of allogenic MHC molecules bound to self MHC molecule on host APC

Question 22

• Hyperacute rejection
  
  • Type of Hypersensitivity
  • Mechanism

Answer 22

• Type II
• Pre-Existing Abs reactive with donor tissue and activate compliment

Question 23

• Acute rejection
  
  • Type of Hypersensitivity
  • Mechanism of Action

Answer 23

• Type IV
• STEPS:
  
  • Donor DCs migrate to lymph nodes
  • Stimulate primary recipient response
  • Activated T Cells migrate to organ and cause tissue damage by generating CTLs and causing delayed type hypersensitivity

Question 24

• Chronic rejection
• Type of Hypersensitivity
• Mechanism of Action

Answer 24

• IV
• M2, Macrophages and T cells are involved
• D/t occlusion of blood vessels and ischemia of the organ
• Macrophage infiltration and smooth muscle proliferation
• Indirect pathway
• Abs can be involved
• Non-immunological factors
  
  • ​Ischemia-reperfusion damage
  • Recurrence of the disease
  • Effects of nephrotoxic drugs

Question 25

• Graft versus host response
• Type of hypersensitivity
• Mechanism of Action

Answer 25

• IV
• Donor T cells in graft proliferate and attack recipient tissue via perforim/granzyme or Fas/Fas L mechanism