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micro exam 3 > Transplant Immunology and Immunodeficiency disease > Flashcards

Transplant Immunology and Immunodeficiency disease Flashcards

1
Q

What is Hypersensitivity

A

Altered immunologic response to an antigen resulting in disease and damage to a host

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2
Q

Types of Hypersensitivity

A

Allergy
Autoimmunity
Alloimmunity

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3
Q

What is an allergy

A

deleterious effects of hypersensitivity to environmental (exogenous) antigens

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4
Q

what is Autoimmunity

A

Disturbance in immunologic tolerance of self-antigens with damage to self tissue

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5
Q

what is Alloimmunity

A

Immun reaction to tissues of another individual

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6
Q

How is Hypersensitivity characterized

A

by the immune mechanism

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7
Q

Types of Hypersensitivity

A

Type I
Type II
Type III
Type IV

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8
Q

type I hypersensitivity

A

IgE mediated

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9
Q

Type II hypersensitivity

A

Tissue-specific reactions

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10
Q

Type III hypersensitivity

A

Immune complex mediated

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11
Q

Type IV hypersensitivity

A

Cell mediated

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12
Q

When the Immune system reacts with antigens on the tissue of other genetically dissimilar members of the same species

A

Alloimmunity

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13
Q

When the Fetus expresses parental antigens not found in the mom

A

Transient neonatal alloimmunity

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14
Q

What are the types of Alloimmunity

A

Transient neonatal alloimmunity
Transplant rejection
Transfusion reactions

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15
Q

What is MHC essential for

A

Antigen presentation to T cell

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16
Q

What do T cells look for

A

Foreign antigens

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17
Q

Self MHC + foreign Ag

A

T cell response

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18
Q

Self MHC + Self Ag

A

No t cell response

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19
Q

Where is MHC expressed

A

it is expressed or can be induced to be expressed on nearly every nucleated cell in the body

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20
Q

MHC I in response to Virus

A

Viruses can infect virtually any nucleated cells so MHC I fnction to alert the CD8+ T cells

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21
Q

what does MHC expression tell the immune system when it sees a self cell

A

it says, yo don’t fuck this cell up, its you.

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22
Q

What is a key factor in determining tissue match for transplant donors and recipients

A

MHC

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23
Q

Specificity of MHC

A

Many different pepetides can bind within the MHC binding cleft with broad specificity

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24
Q

Binding rate of PEptides to MHC

A

Slow on and Slow off rate

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25
Q

Do MHC molecules discrimate from self and foreign peptides

A

NO

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26
Q

what determines which peptides bind and how peptides bind to MHC

A

MHC haplotypes of an individual

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27
Q

what is MHC also known as

A

HLA (human Leukocyte antigen)

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28
Q

how many alleles for MHC genes are there

A

Highly polymorphic (10^13 combinations) as the most polymorphic gene in the human genome

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29
Q

problem with MHC being highly polymorphic

A

Hard to find transplant donors even under 1st degree relatives

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30
Q

How are MHC alleles expressed

A

Concomitantly

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31
Q

the set of MHC alleles on an individual chromosome

A

MHC haplotype

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32
Q

What can the MHC haplotype influence

A

how an individual responds to certain pathogens
Susceptiblity to certain diseases
Transplant success

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33
Q

Different types of transplant rejection classified according to time

A

Hyperacute
Acute
Chronic

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34
Q

how does Hyperacute graft rejection occure

A

Immediately due to preexisting antibody to the antigens on teh graft

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35
Q

Commonality of hyperacute graft rejection

A

rare

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36
Q

How does Acute GRaft rejection occure

A

Cell-mediated response against unmatched HLA antigens

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37
Q

When does Chronic Graft rejection occur

A

Months or years

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38
Q

what is the cause of Chronic GRaft rejection

A

Inflammatory damage to endothelial cells of vessels due to a weak cell-mediated reaction against minor HLA antigens

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39
Q

what is the result of Hyperacute rejection

A

Complement activation
endothetlial damage
Inflammation
thrombosis

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40
Q

what is the result of an acute rejection

A

Parenchymal cell damage
Interstitial inflammation
Endothelialitis

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41
Q

what is the result of ionchronic rejection

A

Chronic DTH reaction in vessel wall
Intimal smooth msucle cell proliferation
Vessel occlusion

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42
Q

who is at risk for Graft-Versus-Host (GVH) Disease

A

Immunocompromised individuals (not a problem in Immunocompetent people)

43
Q

what are the T cells capable of in grafts

A

They are mature and capable of cell-mediated destruction of tissues in the recipient

44
Q

What are Transfusion reactions

A

Antibodies agisnt blood group antigens

45
Q

how are a and B blood antigens expressed

A

Codominant

46
Q

what antibodies do people have in response to a or B blood type

A

antigens to antibodies to whatever they lack

47
Q

how are anti-a and anti b antibodies produce

A

Made by similar antigens on naturally occuring bacteria in the intestinal tract

48
Q

what class are antibodies for A and B blood type

A

IgM

49
Q

Universal donor

A

O blood type

50
Q

Universal acceptor

A

AB blood typ

51
Q

history of Immunodeficiency discription

A 
Hippocrates: 400 bc
Da Vinci: 1510 AD
Traygdon Wilsmyth: 1770
Louis PAstuer: 1880
Ogden Bruton: 1950
52
Q

what was the first primary immunodeficiency disease to be described

A

Bruton Agammaglobulinemia

53
Q

What did Colonel Ogden Bruton note

A

1952, absence of Immunoglobulins in a boy with a history of pneumonias and other bacterial infections
First physican to provide specific immunotherapy for X linked disorder by administering intramuscular injections of IgG

54
Q

Types of Immunodeficiencies

A

PRimary/Congenital Immunodeficiencies

Secondary/acquired immunodeficiencies

55
Q

What are Primary/Congenital immunodeficiencies

A

Genetic defects that result in an increased susceptibility to infection

56
Q

when do Primary/COngenital Immunodeficiences manifest

A

In infancy and Childhood

57
Q

How many people have Primary or congenital immunodeficiencies

A

1:500 in the US

58
Q

what do Secondary or acquired Immunodeficiencies develop as

A 
As a consequence of:
Malnutrition
Disseminated Cancer
Treatment with immunosuppressive drugs
Infection of cells of the immune system
59
Q

how common are Toll-Like receptors

A

Conserved across widely diverse species

60
Q

What can Primary immunodeficiency disorders affect

A

one+ components of the immune system

T, B lymphocytes, NK cells, Phagocytic cells and complement proteins

61
Q

Immunodeficiencies from Primary Immunodiciencies may result from what

A

Defects in leukocyte maturation, activation from defects in effector mechansisms of innate and adaptive immuntiy

62
Q

what is the principle consequence of an immuno-deficiency

A

INcreased susceptibility to infection

63
Q

What determines the nature of the infection due to an immunodeficiency

A

Depends on the componenent of the immune system that is defective

64
Q

Deficient humoral immunity results in

A

Increased susceptibility to infection by pyogenic bacteria

65
Q

other name for X-linked Agammaglobulinemia(XLA)

A

Bruton’s Agammaglobulinemia

66
Q

What is XLA

A

All antibody isotypes are very low (not even IgM or IgD)
Circulating B cells are absent
PRe-B cells are present in reduced numbers in bone marrow

67
Q

What happens to the tonsils and lymph nodes due to XLA

A

Tonsils are usualy very small

Lmph nodes rarely palpable due to lack of gerinal center

68
Q

Thymus changes due to XLA

A

Architecture is normal b/c t-cell dependent areas of spleen and lymph nodes

69
Q

Why do boys with XLA remain healthy for the first 6-9 months of life

A

Maternally transmitted IgG antibodies

70
Q

What happens after a while for guys with XLA

A

Get a lot of extracellular pyogenic organisms infections

71
Q

What is the defect due to XLA

A

Loss of function of Bruton Tyrosine Kinase

72
Q

Roll of Bruton Tyrosine Kinase

A

Pre-B cell expansion and maturatio into Ig-expressing B cells

73
Q

What characterizes X-linked immunodeficiency with Hyper-IgM

A

Low serum IgG, IgA, and IgE

High levels of polyclonal IgM

74
Q

When do patients with Hyper-IgM become symptomatic

A

after the 1st or second year of life with recurrent pathogenic infections

75
Q

How are patients with XLA different than that of Hyper-IgM

A

Hyper IgM patients have lymphoid hyperplasia

76
Q

What is the defect in X-linked immunodeficiency with hyper-IgM

A

Loss of CD40 ligand (CD154) that is expressed on helper T cells

77
Q

What does Loss of CD40 ligand (CD154) lead to

A

Prevents the T cell from co-stimulating antigen-specific B cells (through CD40)
B cells are not signalted be the T cell to go through isotype sqitching and only produce IgM

78
Q

How to treat immunodeficiencies for humoral immune response

A

Routine – prophylactic antibiotics and/or gamma-globulin therapy

79
Q

What results in increased susceptibility to viruses and other intracellular pathogens

A

Deficient Cell-mediated Immunity

80
Q

How to treat defects associated with deficient T cell responses

A

It is very hard to treat

81
Q

How long can people live with Defects in T-cell function

A

Not long, rarely past infancy or childhood

82
Q

Commonality of X-linked Recessive Severe Combined Immunodeficiency disease

A

Rare

83
Q

What is a Severe combined Immunodeficiency

A

A rare, fetal syndrome characterized by profound deficiencies of T- and B-cell function

84
Q

what is the most common form of Severe combined Immunodeficiency(SCID)

A

X linked SCID(XLSCID)

85
Q

When do people present XLSCID

A

Within the first few months of Life

86
Q

Symtpoms of XSCID in early life

A

Diarrhea, pneumonia, otitis, sepsis, cutaneous infections

87
Q

growth of someone with XLSCID

A

may be normal initially, but extreme wasting usually develops after infections and diarrhea begins

88
Q

What do people with XLSCID often have

A

Persistent infections due to opportuistic organisms (candida albicans, pneumocysits carinii, varicella, measles, parainfluenzae, cytomegalovirus, ebv)

89
Q

Can infants with XLSCID get grafts

A

Lack the ability to reject foreign tissue and therefore are at risk for GCHD

90
Q

when can GVHD ocure in XLSCID

A

when maternal T cells cross into fetal circulation while the SCID infant is in utero

91
Q

What cells do XSCID patients lack

A

They have few or no T cells and NK cells

92
Q

What cells do XSCID patients have a lot of

A

B cells ( don’t produce immunoglobulin normally, even after T cell reconstitution by bone marrow transplantation)

93
Q

what are the aims of current treatments for Immunodeficienceies

A
  1. Minimize and control infections

2. replace the defective or absent components of the immune system by adoptive transfer and or transplantation

94
Q

What is valuable for agammaglobulinemic parients to save their lives

A

Passive immunization with pooled gamma globulin

95
Q

what is the treatment of choice for various immunodeficiency disease

A

Bone marrow transplantation

96
Q

Successfulness of Bonemarrow transplantation

A

it can treat SCID and other similar diseases

97
Q

Short lived Cellular reservoir of HIV

A

CD4+ T cells for the first phase of decay with a half life of 1 day

98
Q

Productively infection long lived cells for HIV

A

Monocytes and macrophages for the second phase of decay with a half life of 2 weeks

99
Q

Productively infected resting memory cells for HIC

A

Resting/memory CD4+ cells as the 3rd phase of decay greater than 50 years

100
Q

Progression of HIV

A

Primary infection of cells in blood, mucosa
Infection established in lymphoid tissues (lymph node)
Acute HIV syndrome, spread of infection throughout the body
Immune response
Clinical latency
AIDS

101
Q

Acute HIV syndrome with spread of infectionthroughout the body

A

Viremia

102
Q

Immue response to HIV effectiveness

A

PArtial control of viral replication

103
Q

What happens during the Clincial latency of HIV

A

Estblishment of Chronic infection
Virus trapped in lymphoid tissues by folicular dendric cells
low level viral production
then more microbial infections leads to increased viral replicaion

104
Q

what happens with AIDS

A

Destruction of Lymphoid tissues

Depletion of CD4+ T cells

micro exam 3 (15 decks)

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