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MOD Exam II > (1) Diseases of the Immune System I (Singh) > Flashcards

(1) 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
The diversity of HLA haplotypes inherently causes differences in the pouplation in terms of:
Fighting off illness Allergic sensitivities
26
How are **HLA haplotypes** clinically important?
Must consider with: - Transplanted organs - Associated autoimmune diseases
27
Summarize cell-mediated immunity
APC's bring back pathogens while expressing **MHC-associated peptide antigens** Recognized by T cells to elicit targeted response via: - Proliferation - Differentiation - Migration - Killing
28
MHC Class I Kill what? By what cells?
Intracellular pathogens CD8+ cells
29
MHC Class II Kill what? By what cells?
Extracellular pathogens CD4+ *recruitment* of macrophages and other T lymphocyte subsets
30
**B lymphocytes** are responsible for what type of immunity?
Humoral immunity (Antibody production)
31
Antibodies come from \_\_\_\_\_\_\_\_\_ Which come from \_\_\_\_\_\_\_\_\_
Antibodies come from **plasma cell**s Which come from **B lymphocytes**
32
In order for the humoral immune response to be fully functional, you need the ___________ to be intact
Helper T Cells
33
What are the two aspects of **humoral immunity** that are **_T cell dependent?_**
Isotype switching Increasing affinity
34
Antibody Class Features IgM
The first Ig produced Pentamer --- REALLY BIG Does NOT cross the placenta
35
Antibody Class Features IgG
- Longest half life - Important in fetal protection - Crosses the placenta
36
Antibody Class Features IgA
Mucosal defense Present in high levels in the **colostrum** (first breast milk produced by mom)
37
Antibody Class Features IgE
_-Shortest half life_ _-_Regulates **hypersensitivity reactions** -High affinity binding to FC receptor on mast cells, basophils, eosinophils
38
NK cell -- innate immunity Descibe the activity of NK cells
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
39
Describe **clonal selection**
- 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
40
# Define: Hypersensitivity reaction
An immune reaction to foreign or self antigens that are Excessive Harmful
41
What are the 4 mechanisms of hypersensitivity reactions?
42
What are examples of OBVIOUS hypersensitivity reactions that you can idendify based on presentation?
- Anaphylaxis - Asthma attack - Granuloma
43
What are examples of SUBTLE hypersensitivity reactions that require you know what is happening immunologically to diagnose?
- Goodpasture syndrome - Lupus erythematosus - Type 1 DM
44
What is included in a **Type I Hypersensitivity** reaction?
Seasonal allergies Asthma Food allergies Severe allergic reactions (urticaria, angioedema, anaphylaxis)
45
What happens PRIOR to a **Type I Hypersensitivity reaction** occuring (behind the scenes)?
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
46
After the priming step for Type I hypersensitivity, what happens with a **repeat exposure to the allergen?**
Mast cell activation: Degranulation (Histamine) Lipid mediators (Leukotrienes B4, C4, D4, prostaglandin D2, platelet activating factor)
47
What are (3) clinical manifestations of mast cell activation?
Bronchoconstriction Bowel peristalsis increases Vasodilation permeability increases
48
What are the two phases of a **Type I Hypersensitivity reaction?**
Immediate reaction Late reaction
49
What is occuring in the **_immediate reaction_** of a **Type I Hypersensitivity reaction?**
Mast cell mediators are active!!! Vasodilation Vascular leakage Smooth muscle spasm
50
What is occuring in the **_late reaction_** of a **Type I Hypersensitivity reaction?**
Inflammatory cells are active!!! Eosinophils Basophils Neutrophils \*Epithelial damage
51
What is this?
Eosinophilic esophagitis - Food allergy - Recurrent dysphagia - Weight loss (hurts to swallow)
52
How do you determine the allergen that is causing an allergic reaction?
Skin prick testing
53
Describe what a **Type II Hypersensitivity Reaction** is:
Reactions where **antibodies** directly react with antigens present on the cell surface or extracellular matrix
54
How many mechanisms are there for **Type II Hypersensitivity?** What are they called?
3 A. Opsonization and **phagocytosis** B. Complement **(inflammation)** C. Antibody-mediated **cellular dysfunction**
55
Describe the: Opsonizatinon and phagocytosis Mechanism of a **Type II hypersensitivity reaction**
Opsonization leads to **phagocytosis** Basic mechanism: no cells! Anemia, thrombocytopenia
56
Describe the: Complement Mechanism of a Type II hypersensitivity reaction
Basic mechanism = Damaged Tissue! Inflammation and tissue injury caused by **neutrophils**
57
Describe the mechanism of **rheumatic heart disease**
Combination of **Type II hypersensitivity rxn** and **molecular mimicry** Body is attacking cardiac tissue mistakingly thinking it is **streptococcal** antigen
58
Describe the: Antibody-mediated cellular dysfunction Mechanism of a Type II hypersensitivity reaction
Basic mechanism = Dysfunction due to **receptor blockade** - Disrupted endocrine signaling - Disrupted neural signaling
59
Describe **Type III Hypersensitivity reaction** mechanism
Antigen-antibody complexes **form** and **deposit** causing _damage_
60
Which form of hypersensitivity is commonly associated with **"Serum sickness"?**
Type III
61
Which is Type II vs Type III?
62
What is the mechanism of **Type IV hypersensitivity** reactions?
T-cell mediated!!! CD4+ responds by: releasing cytokines and inducing inflammation CD8+ responds as a cytotoxic agent against antigens on surface of target cell
63
What is a VERY COMMON DISORDER that is a **type IV hypersensitivity reaction?**
Type I DM
64
What is the major hallmark of a **Type IV hypersensitivity reaction?**
Granuloma!!!
65
Tuberculosis test : the Mantoux test is an example of a Hypersensitivity type ______ reaction
IV
66
Rapid fire Hypersensitivity types: _Anaphylaxis and Asthma attack_
Type I
67
Rapid fire Hypersensitivity types: _Granuloma_
Type IV
68
Rapid fire Hypersensitivity types: _Goodpasture syndrome_
Type II
69
Rapid fire Hypersensitivity types: _Lupus Erythematosus_
Type III
70
Rapid fire Hypersensitivity types: _Type 1 DM_
Type IV
71
What is **central tolerance?**
T cells have learned to **tolerate self-antigens** Learned prior to release from generative lymphoid organs
72
What is **peripheral tolerance?**
T cells have learned to tolerate self-antigens; Ongoing regulation in peripheral tissues
73
What are examples of **inhibitory receptors** on T lymphocytes?
CTLA PD-1
74
How do tumors and viruses utilize inhibitory receptors on T cells to their advantage?
By using the **CTLA/PD1** inhibitory receptors when tumors and viruses bind, it effectivley **silences** the T cell from destroying it
75
How is **blockade of PD-1/CTLA-4 signaling** useful clinically?
TUMOR IMMUNOTHERAPY
76
T regulatory cells are...
Foxp3+
77
**_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?
(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**
78
**_IPEX_** What does IPEX stand for? What mutation is involved? What normal process fails in this disease?
IPEX = Immune dysregulation, polyendocrinopathy, enteropathy, X linked Mutation = FOXP3 Process that fails = Dysfunction of **Treg** cells
79
What is an **autoimmune disease?**
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
80
What is **ankylosing spondylitis?**
_Genetically inherited_ inflammatory condiiton of the joints, particularly the spine Inflammation leads to degeneration and then **fusion of the vertebrae**
81
What specific genetic mutation is **ankylosing spondylitis** associated with?
Class I HLA allele **B27**
82
What is the specific gene associated with **Crohns disease?**
NOD-2 gene
83
Describe how **epitope spreading** develops in _oral lichen planus?_
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
84
What does **ANA** stand for?
Anti nuclear antibody
85
What is an ANA test useful for clinically?
ANA is a **sensitive test** for multiple autoimmune diseases If (+), can prompt more *specific testing* to confirm the particular diagnosis
86
What would: Homogenous Speckled Nucleolar Centromere ANA staining patterns look like?
87
Lupus is an autoimmune disease associated with: What are the tendencies for Lupus in terms of affliction?
VAST ARRAY of autoantibodies Genetic association: HLA-DQ Female bias UV light
88
What are clinical manifestations of Lupus?
Malar rash (aka butterfly rash) Discoid rash Hemolytic anemia Arthritis Skin rashes (Tendency toward younger females)
89
What is the **most common** pattern of Lupus nephritis?
Diffuse Lupus Nephritis (Class IV)
90
Diffuse Lupus Nephritis (Class IV) Describe what you would see histologically:
Globeruli show increased cellularity Proliferation of endothelial, mesangial and epithelial cells
91
Skin changes in SLE Describe histoligically what you would see:
**Malar Rash** Basal layer degeneration of the skin As squamous skin cells degenerate, start to see WHITE (indicates damage)
92
What is a major cardiac manifestation of **Lupus?**
**_Libeman-Sacks endocarditis_**
93
What is an **L-E cell?**
A neutrophil or macrophage that ingests the nucleus of a damage cell (Historically, USED to be used to diagnosis of Lupus, but not anymore!)
94
Describe the features of **Discoid Lupus**
Typically just the **face and scalp** are affected (+) ANA (-) Anti-DS DNA
95
What is **Drug-induced lupus?**
Medication-induced breakdown of self tolerance (Procainamide, hydralazine)
96
Drug induced lupus is POSITIVE for what?
Positive ANA Positive **Anti-Histone Ab**
97
What are the high risk HLA linkages in **drug induced lupus?**
Hydralazine confers high risk for DIL w/ **HLA-DR4** allele Procainamide confers high risk for DIL w/ **HLA-DR6** allele
98
What is **Sjogrens syndrome?**
Autoimmune disease resulting in destruction of **lacrimal** and **salivary gland tissue**
99
What are clinical manifestations of **sjogren syndrome?**
Dry eyes Root caries Oral thrush
100
How do you diagnose **sjogren syndrome?**
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
101
What are the two major complications associated with **sjogren syndrome?**
Pulmonary fibrosis Lymphoma
102
What is **systemic sclerosis?**
FIbrosis throught the WHOLE body!!!
103
Describe the histologic changes you would see in **systemic sclerosis**
(Left) = normal (Right) = systemic scelerosis Lack of fatty layer, vascular hyalinization
104
What would you be able to readily see in a patient with **systemic sclerosis?**
105
Also state - the type of staining you would use - Disease process associated with each
A little trick to remember these: **_S_**peckled : **_S_**ystemic Sclerosis **_C**_entromere: _**C_**REST syndrome
106
What is **CREST syndrome?**
Unique form of limited sclerosis w/ additional features
107
Mixed Connective Tissue Disease High titer for? Common presenting feature?
Anti-ribonucleoprotein (RNP) Raynaud phenomenon
108
What is the uniting pathophysiology of **IgG4-related disease?**
IgG4-producing **plasma cells** T lymphocytes --\> **fibrosis** Which leads to eventual fibrotic scarring and irreversible damage to involved areas
109
GOOD JOB
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MOD Exam II (6 decks)

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