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Renal Final > Immunology > Flashcards

Immunology Flashcards

1
Q

What is the major difference between acute kidney injury (AKI) and chronic kidney disease (CKD)?

A

AKI has no structural changes; CKD has kidney damage for > 3 months w/ fibrosis

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2
Q

Why is ischemia a major concern for the kidney? What does ischemic kidney disease lead to?

A
  • Kidneys have high O2 demand due to energy needed to reabsorb solutes
  • metabolic acidosis and ATP depletion -> acute renal failure (ARF)
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3
Q

What are DAMPs?

A

intrinsic damage-associated molecular patterns (aka alarmins) generated by ECM degradation and released by dying parenchymal cells (necrosis)

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4
Q

Name 2 ways that DAMPs lead to inflammation

A
  • C reactive protein (CRP) binds to DAMPs and activates classical complement pathway
  • Immune cells recognize DAMPs via TLRs and induce inflammation
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5
Q

What do dendritic cells upregulate in early and late stages of AKI?

A

Th17 cells in early stages; Th1 cells in late stages

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6
Q

Describe the role of M1 macrophages in kidney disease

A

classically activated by PAMPs and DAMPs through TLRs; create cytokines for acute phase of kidney inflammation

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7
Q

Describe role of M2 macrophages in kidney disease

A

alternatively activated by IL-4 and IL-13 (T cells); produce IL-10 and TGF-B that play important role in tissue repair and fibrosis

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8
Q

How do M2 macrophages lead to fibrosis? What condition is this connected to?

A
  • produces TGF-B -> growth factor for fibroblasts -> myofibroblasts -> produce CT
  • M2 persistently activated in chronic conditions (excessive fibrosis)
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9
Q

What helps Th17 cells differentiate? What do Th17 cells produce?

A

Th17 differentiated in the presence of IL-6 and TGF-B; produces IL-17 (tissue inflammation)

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10
Q

What does IL-17 recruit?

A

recruits neutrophils and facilitates infiltration of monocytes, Th1, and Th17 cells

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11
Q

What role do Tregs have in AKI?

A

anti-inflammatory role by producing IL-10 and TGF-B

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12
Q

What role do C3a and C5a have in AKI?

A

bind to receptors on neutrophils -> activates ROS to destroy cells

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13
Q

Explain Type II hypersensitivity reactions

A

IgG or IgM antibody binds to cellular antigen -> leads to complement activation and lysis

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14
Q

Explain Type III hypersensitivity reactions

A

antigen-antibody complex deposited in tissues -> activates complement -> inflammation and recruitment of neutrophils -> damage to tissues

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15
Q

Describe each of the following: autograft, isograft, allograft, xenograft

A
  • autograft: from one part of the body to another of the same individual
  • isograft: grafts exchanged between different individuals of identical genetics (identical twins)
  • allografts: grafts exchanged between nonidentical members of same species
  • xenografts: grafts exchanged between members of different species
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16
Q

What is the major non-immunological factor of the condition of an allograft?

A

mechanical trauma and ischemia-reperfusion injury

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17
Q

How does damage to an allograft lead to rejection?

A
  • clotting cascade generates fibrinopeptides -> increase vascular permeability and attract neutrophils and macrophages
  • kinin cascade produces bradykinin (vasodilation)
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18
Q

In which types of transplantations is matching donor/recipient not important?

A

non-vascularized tissues: cornea, heart valves, bone/tendon grafts

19
Q

What is on the surface of A type RBCs?

A

A antigens and anti-B antibodies

20
Q

What is on the surface of B type RBCs?

A

B antigens and anti-A antibodies

21
Q

What is on the surface of AB type RBCs?

A

A and B antigens; no antibodies

22
Q

What is on the surface of O type RBCs?

A

no antigens; anti-A and anti-B antibodies

23
Q

Who is generally a good match as a donor and why?

A

pt’s mother -> exposed to child’s antigens against her own during pregnancy w/ no reaction

24
Q

Explain the microcytotoxicity test for pre-formed antibodies

A

recipient serum added to donor cells (bind together) -> complement added -> dye added -> pre-formed Abs present

25
Q

Which class of HLA is more important for transplantation?

A

HLA Class I b/c they are expressed on all tissue cells

26
Q

Explain the microctytotoxicity test for HLA Class I

A

peripheral blood added to HLA antisera (Abs to HLA Ags) -> Ag-Ab complex formed -> activates classical pathway -> lymphocyte lysis detected by staining -> HLA Ag should be identical in donor and recipient (tests 9 different HLA Ags)

27
Q

Explain mixed lymphocyte response (MLR) for HLA Class II

A

donor cells treated w/ radiation (won’t proliferate but APCs for Class I) -> mixed w/ recipient cells -> more proliferation of recipient cells, the less of a match the donor is

28
Q

What is host vs graft response?

A

host’s immune system attacks donor tissue

29
Q

Why does host vs graft response have a stronger response than against pathogens?

A

due to higher frequency of T cells that recognize graft as foreign

30
Q

Different between direct and indirect allorecognition

A
  • direct -> T cells recognize intact allogenic MHC molecules on surface of donor graft
  • indirect -> alloantigens are recognized by recipient MHC Class II after being processed and presented by APCs
31
Q

Describe hyperacute graft rejection and what causes it. Type of hypersensitivity?

A
  • occurs within minutes of transplant due to pre-existing Abs binding to endothelial cells lining blood vessels (ABO incompatibility) -> activate classical pathway -> leads to death of endothelium
  • Type II
32
Q

Describe acute graft rejection and what causes it. Type of hypersensitivity?

A
  • occurs in days to weeks of transplant due to alloreactive T cells that are activated after donor DCs migrate to lymph nodes and stimulate primary immune response
  • Type IV
33
Q

Describe chronic graft rejection and what causes it. Type of hypersensitivity?

A
  • occurs months to years after transplant due to occlusion of blood vessels and ischemia of organ (recurrence of disease); doesn’t respond to immunosuppressive therapy
  • Type IV
34
Q

What is graft vs host disease (GVHD)? What type of transplants is it most common in? Type of hypersensitivity?

A
  • reaction of grafted mature T cells w/ alloantigens of host (HLA usually matched); occurs in immunocompromised recipients
  • occurs in small bowel, lung and liver transplants
  • Type IV
35
Q

What is the CD marker for macrophages?

A

CD14

36
Q

What is the CD marker for neutrophils?

A

CD15+; CD16b+

37
Q

What is the CD marker for dendritic cells?

A

CD80

38
Q

What is the CD marker for T lymphocytes?

A

CD3+ on all T cells

39
Q

What is the CD marker for Th lymphocytes?

A

CD3+; CD4+

40
Q

What is the CD marker for CTL?

A

CD3+; CD8+

41
Q

What is the CD marker for Tregs?

A

CD3+, CD4+, CD25+

42
Q

What do Th1 cells produce?

A

IFN-y

43
Q

What do Th2 cells produce?

A

IL-4, IL-5, and IL-13

Renal Final (2 decks)

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