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Y Immunology > HS rxns, transplant, cell migration (Ben) > Flashcards

HS rxns, transplant, cell migration (Ben) Flashcards

1
Q

Examples of Type III HS rxns

A

Ab-Ag complex mediated…

  • SLE - anti-RNP and anti-cardiolipin Abs
  • Rheumatoid Arthritis - rheumatoid factor Ab
  • Serum Sickness - Abs against anti-venom, etc.
  • Penicillin Allergy - binds to RBCs –> Ab binding
  • Arthus Reaction - local reaction to injected proteins
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2
Q

Examples of Type II HS rxns

A

IgG against cell surface/matrix antigens…

Cytotoxic:

  • Rh incompatibility: erythroblastosis fetalis
  • Drug hypersensitivity: ex: penicillin –> RBC –> IgG

Non-cytotoxic:

  • Graves/Basedow: TSH-R Ab stimulates T3/T4 release
  • Myasthenia Gravis: anti-nAChR Ab
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3
Q

Examples of Type IV HS rxns…

A

2-3 day delayed, T-cell mediated…

  • Contact Dermatitis: poison ivy complexes with skin proteins –> APCs activate T cells –> memory Ts react to poison ivy/skin complex quickly next time (also via Ni)
  • Multiple Sclerosis: T cells against myelin basic protein
  • Hashimoto’s: hypothyroidism, unknown thyroid Ag
  • Type I DM
  • Celiac: rxn against de-amidated gliadin
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4
Q

5 results of complement activation

A
  1. Lysis - via MAC formation
  2. Opsonization - C4b/3b -> CR1-mediated phagocytosis
  3. Inflammation - C3a/4a/5a anaphylatoxins
  4. B cell activation - C3d binds CR2 on B cells
  5. Immune Complex Clearance - RBCs carry C3b bound complexes to spleen/liver macrophages via CR1
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5
Q

4 reasons ABO antibodies are produced under normal conditions

A
  1. Previous contact with foreign blood
  2. Maternal antigen exposure
  3. Carbohydrate antigens of intestinal microbes
  4. Exposure via plant pollens
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6
Q

Describe “hyperacute rejection” of an allogenic graft.

(timescale, mechanism)

A
  • takes minutes - hours
  • usually occurs via ABO, HLA or VEC (vascular endothelial cell antigen) incompatibility
  • ex: endothelial cells express “allo-antigens” which are bound by host antibodies leading to complement activation, inflammation, endothelial damage + thrombosis
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7
Q

What kind of cells are involved in host vs. graft rejection?

A
  • T cells (both CD4 + CD8)
  • NK cells
  • Macrophages
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8
Q

Describe acute rejection against an allogenic graft.

(timescale, mechanism)

A
  • occurs up to 1 month after graft procedure
  • involves endothelitis in which IgG binds alloantigens on endothelium
  • delayed-type (IV) hypersensitivity occurs via CD4+ Th1, CD8+ cells + macrophages
  • causes intense parenchymal damage + interstitial inflammation
  • (no complement activation)
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9
Q

Describe chronic rejection of an allogenic graft.

(timeframe, mechanism)

A
  • occurs months to years after the graft procedure
  • causes fibrosis and vascular sclerosis
  • due to a chronic type IV HS rxn, intimal SM cell proliferation will lead to vessel occlusion
  • (alloantigen-specific CD4+ cells release cytokines which cause SM prolif.)
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10
Q

Describe the general procedure of a bone marrow graft.

A
  1. Donor (usually family) gives marrow cells via pelvic marrow harvest procedure.
  2. Recipient is treated with radiation and/or chemotherapy to achieve “cytoablation” (removal of their own cancerous marrow cells; also prevents HVG disease)
  3. Marrow transplant is applied to recipient intravenously + the transplanted hematopoietic stem cells repopulate the marrow.
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11
Q

What is apheresis?

How is it used in bone marrow transplantation?

A
  • removal of a certain component of the blood + return of the remaining components to circulation
  • can be used to remove HSCs from donor’s peripheral blood, rather than via painful pelvic marrow harvest
  • (2-3% peripherally circulating WBCs are stem cells)
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12
Q

Name 3 molecules involved in the damage caused by Graft vs. Host Disease

A

All are CD8+ cell products…

  1. TNF
  2. FasL - binds FasR to induce apoptosis
  3. Perforin-Granzyme system - perforin makes hole in membrane + granzymes enter to induce apoptosis
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13
Q

List the target cells + organs of acute GVHD

A
  • mostly endothelial cells are damaged
  • main target organs are skin, liver, GI
  • (VEC (vascular endothelial cell) antigens are highly immunogenic –> when these cells are damaged + their antigens released, further damage occurs in surrounding tissues)
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14
Q

What pathological changes are seen in chronic GVHD?

A
  • fibrosis and atrophy of tissues leading to loss of function
  • externally, skin color changes appear, showing up as spots on the skin
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15
Q

What are 2 biological rejection suppression techniques?

A
  1. Donor Selection - genotyping for immunological compatibility (family / internatn’l tranplant lists)
  2. Ex Vivo Graft Manipulation - suppression of immune cells in graft
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16
Q

What are 3 kinds of ex vivo graft manipulation?

A
  1. Steroid Infusion - graft is infused with corticosteroids to downregulate MHC expression
  2. Tolerance Induction - (no details on this…)
  3. Antibodies - e.g. anti-CD28, anti-MHCII, anti-CD4
17
Q

How does cyclosporin work as a pharmaceutical rejection suppression agent?

(What other drug works this way?)

A
  • blocks NFAT, a transcription factor for IL-2 (thus downregulation T cell proliferation)
  • (FK506 also works this way)
18
Q

How do azathioprineandcyclophosphoamide work in pharmacological rejection suppression?

A
  • both block lymphocyte proliferation
  • (azathioprine via purine synthesis inhibition; cyclophosphamide mechanism is… less clear)
19
Q

Other than the drugs already mentioned…

what are 3 methods for pharmaceutical suppression of graft rejection?

A
  1. Monoclonal Abs - most aimed at T-cell depletion, such as anti-CD3 mAb
  2. Corticosteroids - such as prednisone
  3. Other anti-inflammatory agents
20
Q

What are some (6) immunological changes seen in pregnancy?

(too much for one card… just an overview)

A
  1. Th2 shift
  2. HLA-G - a non-classical HLA expressed on fetal-derived placenta cells
  3. Blocking antibodies - bind antigens without inducing immune response, block other Abs from binding
  4. Decrease of CD8+ cells
  5. hCG and IL-6 release from placenta + female GU tract
  6. PIBF - leads to incr. IL-10 and decr. NK cells
21
Q

What role do trophoblast cells play in the fetal antigen presentation + gestational immune tolerance?

A
  • have no MHC-II
  • have monomorphic MHC-I-like HLA-G/E molecules which:
    • don’t present to CD8+ cells
    • block NK cells (normally activated by MHC-I absence)
22
Q

What cytokines + cell types (2) are important in immunosuppression during pregnancy?

A
  • Th2 cytokines - block Th1 type rxns against fetus
  • TGF-beta - multiple suppressive effects
  • Treg - CD4+/CD25+ cells
  • gamma-delta-T cells
23
Q

What important transcription factor is expressed by Treg cells in the decidua during pregnancy?

A

Foxp3

24
Q

When during pregnancy are Treg levels highest?

(this is probably not necessary, just showed up on a graph in lecture, but wasnt mentioned)

A

Treg levels rise slowly to a peak around week 10-11 and then decline slowly again until birth

25
Q

how are pregnancy-related Tregs created?

from what kind of cells?

what general role do they play?

(also not super important… just seen in a lecture figure)

A
  • naive CD4+ cells become Tregs
  • presentation of paternal alloantigens to CD4+ induces differentiation into “pTreg” cells (p=pregnancy?)
  • pTregs ensure embryo/fetal tolerance and vascularization
26
Q

Aside from pTregs, what other kind of cell is important in gestational immune tolerance?

Name 4 mechanisms by which they promote tolerance (less important than just the cell type, also from a lecture figure)

A

gamma delta T cells

  • leave thymus without CD4 or CD8 + present in placental mucosa
  • suppression + cytolysis of effector Ts
  • secrete Th1 antagonizing cytokines
  • cytolysis of APCs
  • block neutrophil infiltration
27
Q

What three sources provide immunosuppresive hormones during pregnancy?

What are the hormones?

A
  1. Maternal - progesterone + estrogen
  2. Placental - hCG
  3. Fetal - alpha-1-fetoprotein
28
Q

What important molecule is stimulated by a maternal hormone during pregnancy and contributes to numerous mechanisms for gestational immunosuppression?

What mechanisms (5)?

A

PIBF - progesterone-induced blocking factor

  • inhibits NK cells
  • increases Th2 cytokines
  • has “anti-abortive” effects
  • inhibits arachidonic acid metabolism
  • increases asymmetric Ab synthesis
29
Q

What are assymetric antibodies?

A

Abs that have an extra glycosylation in the Fab region, causing them to be “blocking antibodies” which bind antigen but do not activate effector mechanisms

30
Q

What is the difference between chemotaxis and chemokinesis?

A
  • Chemotaxis is vectorial meaning it has a specific direction
  • Chemokinesis is random, without specific direction
31
Q

What is haptotaxis?

A
  • chemotaxis in which the attractant is bound to a surface such as the extracellular matrix
  • ex: axonal outgrowth based on the conc. gradient of adhesion sites
32
Q

What are 4 kinds of “professional” chemoattractants?

A
  • chemokines (CC and CXC family)
  • C3a and C5a (“anaphylatoxins”)
  • bacterial N-formyl peptides (FP)
  • arachidonic acid products
33
Q

What are the 4 classes of chemokines + an example of each?

(examples not that important, except one)

A
  • CC - “RANTES”/CCL5 - eos-/baso-/T cell attractant
  • CXC - CXCL8/IL-8 - mostly from macrophages to attract neutrophils
  • CX3CL - “fractalkine”
  • C - “lymphotactine” - attracts T cells
34
Q

Describe the 3 chamber technique for evaluation of chemotactic agents.

A
  • agarose plate with 3 sets of wells
  • in one set, place attractant; in another place cells; in third place neutral control substance
  • measure the “diameter” of the movement of the cells toward the attractant (dA) and control (d<span>C</span>)
  • dA > d<span>C</span> if tested substances is true chemoattractant
35
Q

Describe the 2 chamber method for evaluating chemoattractant strength.

A
  • one chamber = cells
  • other chamber = chemoattractant
  • between them = semi-permeable membrane
  • after some time, can count # of cell that migrated across membrane to chemoattractant
36
Q

In assays of transendothelial migration …

what is the difference between direct and reverse TEM assays?

A
  • direct - migrating cells placed directly on endothelial cell layer, with filters btwn endoth. + chemoattractant
  • reverse - cells placed directly on filters with endothelial cells below (measures what conc. of chemoattractant needed to “pull” cells thru filter to endothelium)
37
Q

How are migration assays performed on the wall of a cell culture flask?

A
  • coat one side of the flask with ECM peptides
  • load cells onto bottom of flask + let them adhere (24 h)
  • tilt flask and wait 1-10 days as cells culture + migrate
  • can measure migration of cells along ECM peptide layer
38
Q

Describe the “matrigel” technique for in vivo cell migration measurement.

A
  • a gel disk containing chemoattractant (+ sandwiched btwn a thick and thin filter) is inserted into a test animal subcutaneously
  • wait 5-10 days to allow cell migration to occur
  • remove disk, wash with NaCl, fixate + evaluate amt of cells which have migrated into it
39
Q

How can sephadex beads be used to measure in vivo cell migration?

A
  • inject chemoattractant-infused beads into test animal peritoneal cavity
  • wait 6-48 hrs
  • observe granulocyte/monocyte migration into peritoneal cavity + presence of cytokines (LTB4, TNF-a, IL8)

Y Immunology (18 decks)

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