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MI Immuno/Heme > Immune Regulation, transplant immunity, and Hypersensitivity > Flashcards

Immune Regulation, transplant immunity, and Hypersensitivity Flashcards

1
Q

B-1 Cells

A

Do not interact w/ CD4+ Th cells - do not form germinal centers

Mediate responses to T cell independent Ag (i.e. repeateing subunit, pathogen capsular polsaccharides) - some Ag that can crosslink a large number of BCRs simultaneously

B-1 cells are rare in infants but increase in number until ~5 y/o (infants respond poorly to purified capsular polysaccharide Vax - S. pneumoniae and H. influenzae susceptible)

B-1 cells rapidly secrete IgM after activation

Also do not class switch and do not produce memory B cell

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2
Q

What type of infections are asplenic individuals susceptible to?

A

Infections with encapsulated bacterial pathogens -

anticapsular IgM is made by splenic B-1 cells - promoting complement-mediated C3b-opsonization of encapsulated microbes

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3
Q

S. pnuemoniae and clinical consequences of B-1 cells and TI Ags

A
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4
Q

Secondary immune responses and immunologic memory

A
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5
Q

Ab feedback inhibition

A
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6
Q

BCR/FcgR
simultaneous
engagement

A

Inhibits activation of memory B cells

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7
Q

Erythroblastosis fetalis (or hemolytic disease in newborn after birth)

A

Caused by ABO or Rh incompatability

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8
Q

Hb recycling

A
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9
Q

Fas/FasL

A

Fas = death receptor

T/B cells become more sensitive to Fas-mediated killing if they remain activated for a long period of time (AICD = activation-induced cell death)

FasL - main mech for removal of unwanted lymphocytes during development

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10
Q

Autoimmune lymphoproliferative syndrome (ALPS)

A

Defects in Fas or FasL

Chronic, non-malignant lymphoproliferative disease

ALPS results from failure to kill activated and self-reactive T/B cells

Pt’s present w/ enlarged lymph nodes, spleen and/or increased incidence of autoimmune

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11
Q

Rogam

A

IgG to Rh factor - preventing maternal Abs from binding to fetal RBCs - by activating Ab feedback

Turns off naive B cells - would turn on membory T cells

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12
Q

How do APCs turn old effector T cells off?

A

Old T cells will express CTLA-4 or PD-1 on their surfaces - engaged by APC B7 or PD-1L

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13
Q

What drives development of CD4+ Th0 to Treg cells?

A

Exposure of a CD4+ Th0 cell to TGF-beta during activation promotes production of the FoxP3 transcription factor - drives development

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14
Q

Immune dysregulation polyendocrinopathy enteropathy (IPEX)

A

Genetic defects in the FoxP3 gene - primary immunodeficiency

Fatal autoimmune disorder directed against variety of tissues

Autoimmune polyendocrinopathy (early-onset insulin-dependent diabetes mellitus, autoimmune thyroiditis, and/or autoimmune hemolytic anemia/thrombocytopenia

Typical IPEX Pt is a young male presenting w/ enlargement of the secondary lymphoid organs, insulin dependent diabetes, nail dystrophy, and autoimmune dermatitis

Illustrates importance of Treg in maintaining tolerance and protecting against autoimmune

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15
Q

What cytokines do Tregs produce that suppress activity of other effector CD4+ T cells?

A

IL-10 and TGF-beta

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16
Q

Tregs in the gut mucosa

A

Th2 dominant environment

Mucosal DC in MALT promote Th0 to Th2 differentiation

Mucosal macrophage have reduced signaling activity between PRR and NF-kappabeta - results in less inflammatory cytokine production in response to PAMPs

IL-10 dampens Th1 responses - limits immune responses to food and normal microbial flora

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17
Q

GM-CSF and IL-3

A

Stimulate growth and differentiation of bone marrow stem cells

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18
Q
A
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19
Q

IL-5

A

Increases eosinophil production from the bone marrow

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20
Q

Neuro-endocrine regulation of innate and adaptive immune responses

A

TNF-alpha, IL-1beta, and IL-6 cross BBB and stimulate hypothalamus to release CRH

Increases cortisol release which acts on macrophages glucocorticoid receptors to reduce inflammatory cytokine gene transcription

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21
Q

T-cell negative selection

A
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22
Q

T cell clonal anergy and failure of clonal ignorance at an immune privileged anatomical site

A
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23
Q

Type I hypersensitivity reaction

A

Starts immediate - peaks 30 minutes

Ag-specific IgE binds to Fcepsilon receptor-I (FceRI) on surface of mast cells, activated eosinophils, and basophils

  • MOST Importantly – most hypersensitivity reactions require sensitization – pre-exposure to the antigen eliciting the response.
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24
Q

Type II hypersentivity reaction

A

Ag-specific IgG (and/or IgM) = starts 1-2 hrs, peaks at 4-6 hrs.

Binds to ECM or host cell surface-associated allergen

ECM or cell surface-bound allergen-Ig complexes activate complement, release anaphylatoxins, and inflammation, which mediate the reaction

  • MOST Importantly – most hypersensitivity reactions require sensitization – pre-exposure to the antigen eliciting the response.
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25
Q

Type III hypersensitivity reaction

A

Ag specific IgG (and IgM) = 1-2 hours, peaks 4-6 hrs

Binds to soluble allergen in blood or tissue spaces

Immune complexes precipitate on vessel walls - particularly in the skin, renal glomeruli, and joins, which activates complement

  • MOST Importantly – most hypersensitivity reactions require sensitization – pre-exposure to the antigen eliciting the response.
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26
Q

Type IV hypersensitivty reactions

A

Delayed type hyersensitivity = starts 24-hrs and peaks 48-72 hrs

Ag specific effector T-cells (usually Th1, Th17 and/or CD8+ CTL) react against either soluble or cell-associated allergens, which induces inflammation and mediates the hypersensitivty reacdtion

  • MOST Importantly – most hypersensitivity reactions require sensitization – pre-exposure to the antigen eliciting the response.
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27
Q

Examples of IgE-mediated allergic rx’ns

A
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28
Q

Sensitization immediate response

A
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29
Q

Sensitization late response

A
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30
Q

Asthmatic response to inhaled allergen

A
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31
Q

Clinical presentation and location of allergen exposure

A
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32
Q

Type II Penicillin hypersensitivty

A
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33
Q

Type IV reactions and tuberculin rx’n

A
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34
Q

What receptors are upregulated as CD4+ in “old” T cells

A

CTLA-4 and PD-1

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35
Q

Factors that allow Treg cells to inactivate self-reactive effector CD4+ T cells

A

FasL, FoxP3, TGF-beta receptor

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36
Q

AIRE transcription

A

Autoimmune regulator - expression of tissue specific Ag presented by interdigitating DCs or epithelial cells ectopically expressing antigens specific to other tissues

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37
Q

Where does class switching occur?

A

The germinal center of secondary lymhpoid tissue

Why B-1 cells do not class switch, undergo affinity maturation

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38
Q
A

A. Eosinophils

IL-5 is involved in making eosinophils and activating them

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39
Q
A

B. Recurrent infections

Blocking B7 = APCs expressing B7 co-stimulatory factor is needed to activate T cells (binds to CD28 on Tcell to activate it)

Also binds CTLA-4 (expressed by aging T cells) - to undergo apoptosis

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40
Q

An immunological hypersensitivity reaction that occurs within 30 minutes of antigen exposure is classified as which type of hypersensitivity?

A

Type I

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41
Q
A

Type IV hypersensitivity

42
Q

In Type I hypersensitivity, the cytokine IL-4 is directly involved in?

A

Ab class switching in activated B cells

Also drive T cells to Th2 cell differentiation

In type II - IL-4 is involved in complement activation following allergen engagement

43
Q
A

Complement C3b

IgG formed after initial response = hemolytic anemia/thrombocytopenia

44
Q

An outdoorsman has been bitten by a rare, but very venomous snake. The only therapeutic option is to administer antivenin generated in horses. About 5-days after the injection, the patient begins to experience fever, vasculitis, arthritis, and nephritis. This immunological reaction is best described as?

A

Type III hypersensitivity reaction

(deposition of immune complexes - soluble Ag)

45
Q
A

MHC Class II

46
Q

A healthy person with a newly diagnosed allergy to cat dander visits a home with many cats. Thirty minutes after arrival, the person is having difficulty breathing because of airway constriction. The person leaves the home and symptoms improve; however, 8-hours later the symptoms return and stay about 4-5 hours. This type of immunological reaction at the 8-hour stage is best described as:

A. Reaction primarily caused by histamine release

B. Reaction caused by the production and release of leukotrienes

C. Reaction involving pre-formed memory Th1 cells

D. Reaction involving pre-formed IgG Abs specific to Ag

A

B. Reaction caused by the production and release of leukotrienes

47
Q

Which granulocyte involved in hypersensitivity reactions does not constituively express the IgE receptor?

A

Eosinophils

Produce major basic protein - toxic to multicellular parasites and host cells

48
Q

Study

A

Study

49
Q
A

C. Mast cells

50
Q
A

E. Histamine

51
Q

Late phase mast cell response

A
52
Q
A

B and D - Basophils and Mast cells

53
Q

Eosinophils

A
54
Q

Control of Eosinophil response

A
55
Q
A

B. IL-4

56
Q

Allergen desensitization

A

IgG4 is involved in a down regulation of the inflammatory response

57
Q
A

C. IgG

Same as Type III

IgE in type I

Memory T cells in Type IV

58
Q
A

D. Hapten

59
Q
A

C. IgG

60
Q

What favors the formation of small immune complexes?

A

When Ag conc.&raquo_space;> Ab con.

61
Q

Pathology of Type III hypersensitivty reactions

A
62
Q

Arthus reaction

A
63
Q

Type IV hypersensitivity

A

I.e. poison ivy, toxic metal contact dermatitis, and tuberculin rx’n

64
Q

Tuberculin reaction

A
65
Q

Type IV hypersensitivity to metals

A
66
Q

Transplantation antigens

A

HLA class I and II; MHC

67
Q

Alloantigens

A

Antigens that vary between members of same species

68
Q

Alloreactions

A

Immune response provoked by alloantigens

69
Q

Graft-vs-host-disease (GVHD)

A

Alloreaction that arises from mature T cells in the grafted bone marrow (or rarely in solid organs) that attack and reject the recipients health tissue

70
Q

Types of transplants

A

Autologous
Syngeneic (transplant between identical twins; inbred animals)
Allogeneic (human to human; not identical twins)
Xenogeneic (pigs most suitable)

71
Q

Ags responsible for transplant rejection

A

ABO and Rh D

HLA-human leukocyte Ag (MHC I/II)

Minor histocompatibility Ags: Non-MHC, normal cellular proteins - rx’n not as severe as allo-MHC mediated rejections

RBCs do not have HLA Ag’s

72
Q

Direct Coomb’s test

A

Detects in vivo Ab/RBC Ag rx’ns

73
Q

Mixed lymphocyte Rx’n test for potential transplant rejection

A
74
Q

Hyperacute transplant rejection

A

-Caused by pre-existing Abs
-Occurs within hours
-No reliable way of reversing

Abs to ABO or MHC allo-Ags (type II hypersensitivity rx’n) bind to graft vasculature eliciting complement activation

Can be prevented by the “cross-match-assay” to discover allo-reactive Ab

Becuase of typing - does not happen anymore in clinic

75
Q

Acute transplant rejection

A

-Can be cell mediated and/or alloAb mediated
-Caused by recipient allo-reactive CD8 and CD4 T cells specific for inconsistencies in donor MHC from donor DCs
-Takes days to develop
-Can be reduced/prevented w/ immune suppression

-Type-IV hypersensitivity rx’n

76
Q

Chronic transplant rejection

A

-activation of alloreactive Abs and T-cells
-Ultimately results in vascular occlusion and interstitial fibrosis
-Occurs months/years after transplant

77
Q

Mechanisms of Graft Rejection

A

Direct allorecognition/rejection:

DCs of an inflamed transplant undergoing rejection are activated - migrate to lymph where they settle into T-cell zone and present Ag (common in acute rejection)

Indirect:

Some donor-derived DCs that migrate to draining lymphoid tissue die there by apoptosis - membrane frags containing HLA are taken up by recipient DCs

78
Q

Bone marrow transplant

A

Myeloablative therapy - cytotoxic drugs and irradiation to prevent rejection by recipient T cells and kill all hematopoietic cells w/i recipients bone marrow

A critical feature of the T-cells of the patient’s new immune system is their positive selection by thymic epithelial cells expressing

79
Q

Graft-versus host disease in bone marrow transplants

A

Because the number of mature T-cells in the transplant is limited, the duration is usually restricted to the first few months after transplant

Can be easily demonstrated experimentally by the mixed lymphocyte reactionS

80
Q

GVHD tissue reactions and grading and diagnostic sxs

A
81
Q

Autologous bone marrow transplant

A

Commonly used Tx option for lymphomas - unless spread to marrow

CD34-expressing stem cells are separated by leukophoresis after stimulation w/ granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF)

82
Q

ABO Ags

A

Glycoacetyl transferase adds terminal AA

83
Q

ABO Ags and Abs

Chart

A
84
Q

Effect of HLA Matching on Kidney Graft Sruvival

A
85
Q

Cross-matching test

A

Recipient serum and donor RBCs

Positive agglutination shown

86
Q

Indirect Coomb’s test

A

Detects in vitro Ab/RBC Ag reactions (i.e. blood transfusion, antenatal Ab screening)

87
Q

Mixed lymphocyte Rx’n

A

Increased radioactivity = increased proliferation of recipient cells = MHC mismatch

88
Q
A

Thrombosed artery secondary to humoral chronic rejection of kidney

89
Q
A

Direct pathway of allorecognition

90
Q

The type of transplant rejection where pre-existing IgG antibodies in the recipient’s serum reacting to a donor’s solid organ transplant is closest to which type of Hypersensitivity reaction?

A

Type II hypersensitivity reactions

91
Q

A patient has received an allogenic hematopoietic stem cell transplant and is now experiencing a significant rash, increased bilirubin, and diarrhea. Which immune component type is most responsible for this reaction?

A

D) Donor’s T-cells

92
Q

A key event specific to chronic rejection in solid organ transplantation is?

A

E) Interstitial fibrosis

93
Q

A skin graft is performed between two mice with the same genetic background. This type of transplant is called?

A

Syngeneic

94
Q
A

C. RBC autoimmunity

Direct tests for autoimmunity or drug-induced immune-mediated penicillin rx’n

95
Q
A

Acute rejection of heart

96
Q
A
97
Q
A

A. Hyperacute

Type II - IgG mediated hypersensitivty - primary cause of hyperacute rejection

98
Q

Difference in direct vs. indirect allo-recognition of HLA

A
99
Q

Sxs of graft-vs-host disease

A

Maculopapular rash to generalized erythema w/ blistering and desquamation (depending on severity)

Elevated serum bilirubin

Diarrhea (w/ or w/o obstruction in severe cases)

100
Q

CTLA-4

A

Used by APCs

101
Q
A

MI Immuno/Heme (35 decks)

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