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*mod i exam 3 > LECT Diseases of the Immune System I (Singh) > Flashcards

LECT Diseases of the Immune System I (Singh) Flashcards

1
Q

Innate Immunity

What is the general function?

What are the cells involved?

What are the proteins involved?

A

Pre-existing defense against pathogens

Cells: Neutrophils, Dendritic cells, NK cells

Proteins: Complement

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2
Q

Adaptive Immunity

General function?

What are the primary players?

A

Specific, programmed defense in response to antigen presence

LYMPHOCYTES (+antibodies)

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3
Q

Innate Immunity:

What are examples of physical barriers?

A
  • Skin
  • Lining of tracehal bronchial tree
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4
Q

Innate Immunity:

What are examples of chemical barriers?

A
  • Saliva
  • Tears
  • Acidic pH of stomach
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5
Q

Innate Immunity

What are examples of pattern recognition receptors?

A
  • Toll like receptors
  • NOD-like receptors and the inflammasome
  • C-type lectin receptors
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6
Q

What are the generative organs of the adaptive immune system?

A

Bone marrow

Thymus

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7
Q

What are the functions of the generative organs of the adaptive immune system?

-Bone marrow

-Thymus

A

Bone marrow

-Generation of lymphocyte stem cells

-B lymphocyte maturation

Thymus

  • Maturation of T lymphocytes
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8
Q

What are the peripheral organs/tissues of adaptive immunity?

A

Lymph nodes

Spleen

Mucosa-associated lymphoid tissues [MALT] (tonsils, adenoids, peyer’s pathes)

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9
Q

What are the functions of the peripheral organs/tissues of the adaptive immune system?

Lymph nodes

Spleen

Mucosa-associated lymphoid tissues

A

Lymph nodes

-Lymphocytes can interact w/ APC’s and antigens in circulating lymph

Spleen

-Lymphocytes can interact with blood-borne antigens

Mucosa-associated lymphoid tissues

-Allow lymphocytes and plasma cells to be in the vicinity of antigens within the mouth and intestinal tract

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10
Q

Identify the structures at the arrows

A
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11
Q

Where do B cells mature?

A

Bone marrow

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12
Q

What organ is this?

A

Thymus

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13
Q

What is the overarching function of the thymus?

A

T Cell Training

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14
Q

Describe the maturation process of T cells

A

Cells that are destined to become T cells travel from the bone marrow to the thymus.

These cells start in the cortex, and as they mature, they travel inward toward the medulla (the center).

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15
Q

What is the goal of T cell maturation?

A

Not attack our own tissues

Teaching the T cells what our own MHC molecules look like, SO THEY DON”T ATTACK

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16
Q

What are the histologic features of the thymus?

A

Cortex

-TON of lymphocytes

Medulla

-Hassal corpuscles (squamous cell nests)

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17
Q

Describe the events that occur in the lymph node

A

APC’s interact with lymphocytes

  • T and B cell clonal expansion
  • B cell differentiation into plasma cells
  • Migration of T cells and plasma cells out of lymph nodes and into circulation
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18
Q

T lymphocytes

Give the other name for the following:

Helper

Cytotoxic

Regulatory

A

Helper : CD4+

Cytotoxic : CD8+

Regulatory : Treg

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19
Q

General function of MHC?

A

Display peptides for T-cells in adaptive immunity

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20
Q

Describe MHC Class I

Where located?

What do they typically recognize?

How are they processed?

How are they expressed?

Which cells?

A

ALL nucleated cells (and platelets)

Recognize intracellular antigens (eg viral, tumor)

Processed into peptides by the proteasome

Peptides are transported to the ER, load into the groove of MHC, and the entire complex migrates to the surface

Presentation of complex to CD8+ (cytotoxic) T cells

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21
Q

Describe MHC Class II

Where located?

What do they typically recognize?

How are they processed?

How are they expressed?

Which cells?

A

Located on APCs

Recognize extracellular antigens (bacterial, allergens)

Processed into peptides by the endolysosomal enzymes

Vesicles form with processed peptides and MHC II complex

Present to CD4+ (Helper) T cells

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22
Q

What is the difference b/w MHC and HLA?

A

Human leukocyte antigens (HLA) are the Major histocompatibility complex molecules that are present in humans

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23
Q

Which chromosome encodes the HLA molecular structure for a given individual?

A

Chromosome 6

*Remember: there are 6 regions we care about.

  • HLA-A
  • HLA-C
  • HLA-B
  • HLA-DR
  • HLA-DQ
  • HLA-DP
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24
Q

How many HLA alleles are there?

A

1000’s

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25
Q

The diversity of HLA haplotypes inherently causes differences in the pouplation in terms of:

A

Fighting off illness

Allergic sensitivities

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26
Q

How are HLA haplotypes clinically important?

A

Must consider with:

  • Transplanted organs
  • Associated autoimmune diseases
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27
Q

Summarize cell-mediated immunity

A

APC’s bring back pathogens while expressing MHC-associated peptide antigens

Recognized by T cells to elicit targeted response via:

  • Proliferation
  • Differentiation
  • Migration
  • Killing
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28
Q

MHC Class I

Kill what?

By what cells?

A

Intracellular pathogens

CD8+ cells

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29
Q

MHC Class II

Kill what?

By what cells?

A

Extracellular pathogens

CD4+ recruitment of macrophages and other T lymphocyte subsets

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30
Q

Antibodies come from _________

Which come from _________

A

Antibodies come from plasma cells

Which come from B lymphocytes

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31
Q

In order for the humoral immune response to be fully functional, you need the ___________ to be intact

A

Helper T Cells

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32
Q

What are the two aspects of humoral immunity that are T cell dependent?

A

Isotype switching

Increasing affinity

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33
Q

Antibody Class Features

IgM

A

The first Ig produced

Pentamer — REALLY BIG

Does NOT cross the placenta

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34
Q

Antibody Class Features

IgG

A
  • Longest half life
  • Important in fetal protection
  • Crosses the placenta
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35
Q

Antibody Class Features

IgA

A

Mucosal defense

Present in high levels in the colostrum (first breast milk produced by mom)

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36
Q

Antibody Class Features

IgE

A

-Shortest half life

_-_Regulates hypersensitivity reactions

-High affinity binding to FC receptor on mast cells, basophils, eosinophils

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37
Q

NK cell – innate immunity

Descibe the activity of NK cells

A

Activity of NK cells is regulated by activating and inhibiting MHC Class I receptors

Healthy cells will present MHC Class I and will NOT be destroyed by NK cells

Damaged cells will not express MHC Class I and WILL be desstroyed by NK cells

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38
Q

Describe clonal selection

A
  • Lymphocytes are killed if they recognize self antigens (clonal deletion)
  • Best suited lymphocytes that can detect a pathogenic antigen will be selected to be clonally expanded
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39
Q

Define:

Hypersensitivity reaction

A

An immune reaction to foreign or self antigens that are

Excessive

Harmful

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40
Q

What are the 4 mechanisms of hypersensitivity reactions?

A
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41
Q

What are examples of OBVIOUS hypersensitivity reactions that you can idendify based on presentation?

A
  • Anaphylaxis
  • Asthma attack
  • Granuloma
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42
Q

What are examples of SUBTLE hypersensitivity reactions that require you know what is happening immunologically to diagnose?

A
  • Goodpasture syndrome
  • Lupus erythematosus
  • Type 1 DM
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43
Q

What is included in a Type I Hypersensitivity reaction?

A

Seasonal allergies

Asthma

Food allergies

Severe allergic reactions (urticaria, angioedema, anaphylaxis)

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44
Q

What happens PRIOR to a Type I Hypersensitivity reaction occuring (behind the scenes)?

A

DC’s present antigen to naive T cells

T cells differentiate to Th2 cells

B cells class switch to IgE

Mast cells get prepared by binding IgE to specific Fc(epsilon)RI receptor

45
Q

After the priming step for Type I hypersensitivity, what happens with a repeat exposure to the allergen?

A

Mast cell activation:

Degranulation (Histamine)

Lipid mediators (Leukotrienes B4, C4, D4, prostaglandin D2, platelet activating factor)

46
Q

What are (3) clinical manifestations of mast cell activation?

A

Bronchoconstriction

Bowel peristalsis increases

Vasodilation permeability increases

47
Q

What are the two phases of a Type I Hypersensitivity reaction?

A

Immediate reaction

Late reaction

48
Q

What is occuring in the immediate reaction of a Type I Hypersensitivity reaction?

A

Mast cell mediators are active!!!

Vasodilation

Vascular leakage

Smooth muscle spasm

49
Q

What is occuring in the late reaction of a Type I Hypersensitivity reaction?

A

Inflammatory cells are active!!!

Eosinophils

Basophils

Neutrophils

*Epithelial damage

50
Q

What is this?

A

Eosinophilic esophagitis

  • Food allergy
  • Recurrent dysphagia
  • Weight loss (hurts to swallow)
51
Q

How do you determine the allergen that is causing an allergic reaction?

A

Skin prick testing

52
Q

Describe what a Type II Hypersensitivity Reaction is:

A

Reactions where antibodies directly react with antigens present on the cell surface or extracellular matrix

53
Q

How many mechanisms are there for Type II Hypersensitivity?

What are they called?

A

3

A. Opsonization and phagocytosis

B. Complement (inflammation)

C. Antibody-mediated cellular dysfunction

54
Q

Describe the:

Opsonizatinon and phagocytosis

Mechanism of a Type II hypersensitivity reaction

A

Opsonization leads to phagocytosis

Basic mechanism: no cells!

Anemia, thrombocytopenia

55
Q

Describe the:

Complement

Mechanism of a Type II hypersensitivity reaction

A

Basic mechanism = Damaged Tissue!

Inflammation and tissue injury caused by neutrophils

56
Q

Describe the mechanism of rheumatic heart disease

A

Combination of Type II hypersensitivity rxn and molecular mimicry

Body is attacking cardiac tissue mistakingly thinking it is streptococcal antigen

57
Q

Describe the:

Antibody-mediated cellular dysfunction

Mechanism of a Type II hypersensitivity reaction

A

Basic mechanism = Dysfunction due to receptor blockade

  • Disrupted endocrine signaling
  • Disrupted neural signaling
58
Q

Describe Type III Hypersensitivity reaction mechanism

A

Antigen-antibody complexes form and deposit causing damage

59
Q

Which form of hypersensitivity is commonly associated with “Serum sickness”?

A

Type III

60
Q

Which is Type II vs Type III?

A
61
Q

What is the mechanism of Type IV hypersensitivity reactions?

A

T-cell mediated!!!

CD4+ responds by: releasing cytokines and inducing inflammation

CD8+ responds as a cytotoxic agent against antigens on surface of target cell

62
Q

What is a VERY COMMON DISORDER that is a type IV hypersensitivity reaction?

A

Type I DM

63
Q

What is the major hallmark of a Type IV hypersensitivity reaction?

A

Granuloma!!!

64
Q

Tuberculosis test : the Mantoux test is an example of a

Hypersensitivity type ______ reaction

A

IV

65
Q

Rapid fire Hypersensitivity types:

Anaphylaxis and Asthma attack

A

Type I

66
Q

Rapid fire Hypersensitivity types:

Granuloma

A

Type IV

67
Q

Rapid fire Hypersensitivity types:

Goodpasture syndrome

A

Type II

68
Q

Rapid fire Hypersensitivity types:

Lupus Erythematosus

A

Type III

69
Q

Rapid fire Hypersensitivity types:

Type 1 DM

A

Type IV

70
Q

What is central tolerance?

A

T cells have learned to tolerate self-antigens

Learned prior to release from generative lymphoid organs

71
Q

What is peripheral tolerance?

A

T cells have learned to tolerate self-antigens;

Ongoing regulation in peripheral tissues

72
Q

What are examples of inhibitory receptors on T lymphocytes?

A

CTLA

PD-1

73
Q

How do tumors and viruses utilize inhibitory receptors on T cells to their advantage?

A

By using the CTLA/PD1 inhibitory receptors when tumors and viruses bind, it effectivley silences the T cell from destroying it

74
Q

How is blockade of PD-1/CTLA-4 signaling useful clinically?

A

TUMOR IMMUNOTHERAPY

75
Q

T regulatory cells are…

A

Foxp3+

76
Q

AIRE gene

What is the purpose of AIRE, and where does it exert its normal function?

What normal process would fail in the basence of normal AIRE?

A

(Autoimmune regulator)

Purpose of AIRE = Stimulates expression of some “peripheral tissue-restricted” self antigens in the thymus and is thus critical for deletion of immature T cells specific for these antigens.

Abnormal AIRE= would cause an Autoimmune polyendocrinopathy

77
Q

IPEX

What does IPEX stand for?

What mutation is involved?

What normal process fails in this disease?

A

IPEX = Immune dysregulation, polyendocrinopathy, enteropathy, X linked

Mutation = FOXP3

Process that fails = Dysfunction of Treg cells

78
Q

What is an autoimmune disease?

A

An immune reaction is directed against a self-antigen

That immune reaction is primarily responsible for a pathologic condition

There is no other pathophysiology responsible

79
Q

What is ankylosing spondylitis?

A

Genetically inherited inflammatory condiiton of the joints, particularly the spine

Inflammation leads to degeneration and then fusion of the vertebrae

80
Q

What specific genetic mutation is ankylosing spondylitis associated with?

A

Class I HLA allele B27

81
Q

What is the specific gene associated with Crohns disease?

A

NOD-2 gene

82
Q

Describe how epitope spreading develops in oral lichen planus?

A

Initial T cell response leads to keratonic lesions in oral and conjunctival mucosa –>

Basement membrane disruption exposes NEW antigenic proteins –>

A secondary B cell response occurs

83
Q

What does ANA stand for?

A

Anti nuclear antibody

84
Q

What is an ANA test useful for clinically?

A

ANA is a sensitive test for multiple autoimmune diseases

If (+), can prompt more specific testing to confirm the particular diagnosis

85
Q

What would:

Homogenous

Speckled

Nucleolar

Centromere

ANA staining patterns look like?

A
86
Q

Lupus is an autoimmune disease associated with:

What are the tendencies for Lupus in terms of affliction?

A

VAST ARRAY of autoantibodies

Genetic association: HLA-DQ

Female bias

UV light

87
Q

What are clinical manifestations of Lupus?

A

Malar rash (aka butterfly rash)

Discoid rash

Hemolytic anemia

Arthritis

Skin rashes

(Tendency toward younger females)

88
Q

What is the most common pattern of Lupus nephritis?

A

Diffuse Lupus Nephritis (Class IV)

89
Q

Diffuse Lupus Nephritis (Class IV)

Describe what you would see histologically:

A

Globeruli show increased cellularity

Proliferation of endothelial, mesangial and epithelial cells

90
Q

Skin changes in SLE

Describe histoligically what you would see:

A

Malar Rash

Basal layer degeneration of the skin

As squamous skin cells degenerate, start to see WHITE (indicates damage)

91
Q

What is a major cardiac manifestation of Lupus?

A

Libeman-Sacks endocarditis

92
Q

What is an L-E cell?

A

A neutrophil or macrophage that ingests the nucleus of a damage cell

(Historically, USED to be used to diagnosis of Lupus, but not anymore!)

93
Q

Describe the features of Discoid Lupus

A

Typically just the face and scalp are affected

(+) ANA

(-) Anti-DS DNA

94
Q

What is Drug-induced lupus?

A

Medication-induced breakdown of self tolerance

(Procainamide, hydralazine)

95
Q

Drug induced lupus is

POSITIVE for what?

A

Positive ANA

Positive Anti-Histone Ab

96
Q

What are the high risk HLA linkages in drug induced lupus?

A

Hydralazine confers high risk for DIL w/ HLA-DR4 allele

Procainamide confers high risk for DIL w/ HLA-DR6 allele

97
Q

What is Sjogrens syndrome?

A

Autoimmune disease resulting in destruction of lacrimal and salivary gland tissue

98
Q

What are clinical manifestations of sjogren syndrome?

A

Dry eyes

Root caries

Oral thrush

99
Q

How do you diagnose sjogren syndrome?

A

Use Anti-Ro/SS-A and Anti-La/SS-B tests

or

Biopsy of the lip to look for inflammation of minor salivary gland tissue

100
Q

What are the two major complications associated with sjogren syndrome?

A

Pulmonary fibrosis

Lymphoma

101
Q

What is systemic sclerosis?

A

FIbrosis throught the WHOLE body!!!

102
Q

Describe the histologic changes you would see in systemic sclerosis

A

(Left) = normal

(Right) = systemic scelerosis

Lack of fatty layer, vascular hyalinization

103
Q

What would you be able to readily see in a patient with systemic sclerosis?

A
104
Q

Also state

  • the type of staining you would use
  • Disease process associated with each
A

A little trick to remember these:

Speckled : Systemic Sclerosis

_C_entromere: _C_REST syndrome

105
Q

What is CREST syndrome?

A

Unique form of limited sclerosis w/ additional features

106
Q

Mixed Connective Tissue Disease

High titer for?

Common presenting feature?

A

Anti-ribonucleoprotein (RNP)

Raynaud phenomenon

107
Q

What is the uniting pathophysiology of IgG4-related disease?

A

IgG4-producing plasma cells

T lymphocytes –> fibrosis

Which leads to eventual fibrotic scarring and irreversible damage to involved areas

108
Q

GOOD JOB

A

AHHHHHH GIVE YOURSELF A PAT ON THE BACK, YOU EARNED IT WOW

*mod i exam 3 (16 decks)

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