Autoimmunity Flashcards

(68 cards)

1
Q

[3] The autoimmune response may be influenced by:

A
  1. Self tolerance
  2. Genetics
  3. Other endogenous and environmental factors
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2
Q

[2] Self tolerance

A
  1. Central
  2. Peripheral
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3
Q

This occurs in the thymus and bone marrow,
where T and B cells mature. Any CELLS that STRONGLY REACT to self antigens are ELIMINATED through a process called negative selection.

[self tolerance]

A

Central tolerance

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4
Q

This is a BACKUP SYSTEM for any self-reactive
cells that ESCAPE CENTRAL TOLERANCE. In the lymph nodes and spleen, these cells are made inactive or deleted.

[self tolerance]

A

Peripheral tolerance

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5
Q

[2] Genetics

A
  1. Major Histocompatibility Complex (MHC) Genes
  2. Non - MHC genes
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6
Q

For example, the HLA-B27 allele dramatically increases the risk of developing ankylosing spondylitis.

[peripheral tolerance]

A

Major Histocompatibility Complex (MHC) Genes

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7
Q

These genes often regulate critical immune functions, such as T-cell and B-cell signaling and activation, and the maintenance of T regulatory cells. Examples include genes like PTPN22, IL2RA, and CTLA4.

[peripheral tolerance]

A

Non - MHC Genes

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8
Q

[3] Hormonal Influence

A
  1. Estrogens
  2. Androgens
  3. Prolactin
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9
Q

TEND TO PROMOTE Type 2 helper T-cell (Th2) response, which LEADS TO GREATER B-cell activation and antibody production.

[hormonal influence]

A

Estrogens

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10
Q

This HEIGHTENED ANTIBODY activity is believed to increase the risk of autoimmune disease.

[hormonal influence]

A

Estrogens

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11
Q

On the other hand, FAVOR A Type 1 helper T-cell (Th1) response, ACTIVATING cytotoxic T cells.

[hormonal influence]

A

Androgens

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12
Q

A hormone associated with PREGNANCY and LACTATION, can stimulate both humoral and cell-mediated immune responses.

[hormonal influence]

A

Prolactin

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13
Q

This is when a microbe’s antigens closely resemble self-antigens.

[microbial influence]

A

Molecular mimicry

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14
Q

The immune response to the foreign microbe can MISTAKENLY CROSS-REACT with the similar self antigens, LEADING to an autoimmune attack.

[microbial infection]

A

Molecular mimicry

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15
Q

This mechanism DOESN’T REQUIRE structural similarity between antigens.

[microbial infection]

A

Bystander affect

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16
Q

A microbial infection CAUSES a LOCAL INFLAMMATORY response, recruiting immune cells and activating T cells.

[microbial infections]

A

Bystander effect

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17
Q

This expansion of the immune response is also known as “epitope spreading.”

[microbial infections]

A

Bystander effect

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18
Q

Proteins that CAN ACTIVATE NUMBER OF T CELLS AT ONCE, regardless of their specific antigen.

[microbial infection]

A

Superantigens

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19
Q

If some of these T cells happen to be specific for self-antigens, a widespread autoimmune response can be triggered.

[microbial infection]

A

Superantigens

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20
Q

Refers to changes in GENE EXPRESSION that DON’T INVOLVE ALTERATIONS to the DNA sequence itself.

[epigenetics and gene expression]

A

Epigenetics

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21
Q

These CHANGES CAN BE TRIGGERED by environmental factors like TOXINS, DIET, or AGING.

[epigenetics and gene expression]

A

Epigenetics

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22
Q

Epigenetic modifications, such as __________ or ____________, can cause genes to be over- or under expressed.

A

DNA methylation
Histone changes

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23
Q

In the immune system, this can LEAD TO A BREAKDOWN of SELF TOLERANCE and result in autoimmune diseases.

[epigenetics and gene expression]

A

Epigenetics

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24
Q

Environmental factors can also cause post translational modifications to proteins.

[epigenetics and gene expression]

A

Modification of Self Antigens

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25
The immune system may no longer recognize it as "self" and instead launch an immune response against it. [epigenetics and gene expression]
Modification of Self - Antigens
26
[2] Types of Autoimmunity
1. Systemic autoimmune diseases 2. Organ - specific autoimmune diseases
27
[5] Organ - specific autoimmune diseases
1. Hematologic disorders 2. Endocrine disorders 3. Neuromuscular disorders 4. Renal disorders 5. Gastrointestinal disorders
28
[2] Hematologic disorders AI*
1. Autoimmune Hemolytic Anemia 2. Immune Thrombocytopenia Purpura
29
[3] Endocrine disorders GHI*
1. Grave's disease 2. Hashimoto's Thyroiditis 3. Insulin - dependent Diabetes Mellitus
30
[2] Neuromuscular disorders MM*
1. Myasthenia Gravis 2. Multiple Sclerosis
31
[1] Renal disorders
Goodpasture's syndrome
32
[2] Gastrointestinal disorders PP*
1. Pernicious anemia 2. Primary Bilary Cirrhosis
33
[2] Systemic Autoimmune Diseases RSG*
1. Rheumatoid Arthritis (RA) 2. Systemic Lupus Erythematosus (SLE) 3. Granulomatosis with polyangiitis
34
It is a SYSTEMIC RHEUMATIC DISORDER that is characterized by the presence of CIRCULATING IMMUNE COMPLEXES.
Systemic Lupus Erythematosus (SLE)
35
It is most commonly seen in women and persons of African.
Systemic Lupus Erythematosus
36
[2] Causes: [sle]
1. Idiopathic 2. Drug - induced
37
[5] Symptoms of SLE
1. Rash (butterfly) or other skin abnormalities 2. Myocarditis 3. Lymphadenopathy 4. Glomerulonephritis 5. Serositis
38
[2] Diagnosis or SLE
1. ANA Testing 2. The LE Cell Test
39
[2] ANA Testing of SLE
1. The Fluorescent Antinuclear Antibody Test (FANA) 2. ANA Testing by Immunohistochemistry
40
The entire nucleus of the cell stains UNIFORMLY. [FANA]
Homogenous
41
Antibodies to dsDNA, histones, and DNP. [FANA]
Homogenous
42
Found in patients with Systemic Lupus Erythematosus (SLE)and drug-induced lupus, among other autoimmune diseases. [FANA]
Homogenous
43
Staining is stronger and MORE INTENSES around the outer edge of the nucleus, forming an OUTLINE. [FANA]
Peripheral or Rim
44
Primarily caused by antibodies to dsDNA. [FANA]
Peripheral
45
This pattern is HIGLY SPECIFIC for SLE. [FANA]
Peripheral
46
The nucleus is filled with DISCRETE, fluorescent specks. The nucleolus and dividing cell chromatin are UNSTAINED. [FANA]
Speckled
47
Antibodies to extractable nuclear antigens (ENAs). [FANA]
Speckled
48
Can be seen in patients with SLE, Sjögren'ssyndrome, and SYSTEMIC ERRORS. [FANA]
Speckled
49
PROMINENT STAINING of the nucleoli (small structures within the nucleus). [FANA]
Nucleolar
50
Primarily antibodies to RNA and RNP. [FANA]
Nucleolar
51
Mainly found in patients with SCLERODERMA, but also other connective tissue diseases. [FANA]
Nucleolar
52
Numerous distinct speckles are present in the nucleus, typically 46 per cell, representing the chromosomes. [FANA]
Centromere
53
Antibodies to centromere proteins. [FANA]
Centromere
54
Primarily found in patients with CREST syndrome. [FANA]
Centromere
55
Most specific for SLE. [antinuclear antibody interpretation]
Anti ds - DNA
56
Histone is a nucleoprotein that is a MAJOR CONSTITUENT OF CHROMATIN. [antinuclear antibody interpretation]
Anti - histone antibody
57
Drug induce Lupus-w/ ss-DNA [antinuclear antibody interpretation]
Anti - histone antibody
58
SPECIFIC FOR LUPUS, It cannot be found in other autoimmune. [antinuclear antibody interpretation]
Anti - Sm (Smith)
59
Often found in cutaneous manifestations of SLE, especially PHOTOSENSITIVITY and DERMATITIS. [antinuclear antibody interpretation]
Anti SS-A/ Ro and SS-B/ro
60
Highly prevalent in SCLERODERMA and SJOGREN SYNDROME. [antinuclear antibody interpretation]
Anti SS-A/Ro and SS-B/Ro
61
HETEROGENOUS group of antibodies that BIND TO PHOSPHOLIPID ALONE or are complexed with protein. [antinuclear antibody interpretation]
Antiphospholipid antibodies
62
Associated with DEEP VEIN and ARTERIAL THROMBOSIS and with morbidity and pregnancy. [antinuclear antibody interpretation]
Antiphospholipid antibodies
63
Fever And Arthritis [sle, drugs]
Aspirin, Anti-inflammatory drugs
64
Skin Manifestation [sle, drugs]
Hydroxychloroquine or Chloroquine, Tropical Steroids
65
Acute Fulminant Lupus, Lupus Nephritis ,CNS Complications Systemic [sle, drugs]
Corticosteroids
66
A SECOND WAY that microbes might TRIGGER autoimmunity is through a?
Bystander effect
67
Expansion of the immune response to unrelated antigens.
Epitope spreading
68