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IMM Exam 2 > Tolerance & Autoimmunity > Flashcards

Tolerance & Autoimmunity Flashcards

1
Q

Self-antigens

A

an individual’s own antigens

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2
Q

Immunologic tolerance

A

unresponsiveness to self-antigens

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3
Q

Tolerogens

A

antigens that induce tolerance

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4
Q

Immunogens

A

antigens that induce an immune response

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5
Q

Autoimmunity

A

failure of self-tolerance and resulting immune reaction to self-antigens

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6
Q

Location: Tolerogenic self antigens

A

presence in generative organs (some self antigens) induces negative selection and other mechanisms of central tolerance

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7
Q

Location: Immunogenic foreign antigens

A

presence in blood and peripheral tissues (most microbial antigens) permits concentration in secondary lymphoid organs

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8
Q

Tolerogenic self antigens and Accompanying costimulation

A

Deficiency of costimulators may lead to T cell anergy or apoptosis, development of Treg, or sensitivity to suppression by Treg

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9
Q

Immunogenic foreign antigens and Accompanying costimulation

A

Expression of costimulators, typically seen with microbes, promotes lymphocyte survival and activation

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10
Q

Tolerogenic self-antigens and Duration of antigen exposure

A

Long-lived persistence (throughout life); prolonged TCR engagement may induce anergy and apoptosis

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11
Q

Immunogenic foreign antigens and Duration of antigen exposure

A

Short exposure to microbial antigen reflects effective immune response

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12
Q

3 Characteristics of Tolerance

A

Induced

Antigen-specific

Induced during central tolerance OR peripheral tolerance

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13
Q

Generative (central) tolerance occurs

A

in central lymphoid organs

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14
Q

Central tolerance for T cells occurs in

A

thymus

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15
Q

Central tolerance for B cells occurs in

A

bone marrow

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16
Q

Mechanisms of Central Tolerance for T cells

A

Deletion (- selection)

Regulatory T cells

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17
Q

Mechanisms of Central Tolerance for B cells

A

Receptor editing

Anergy

Deletion

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18
Q

Peripheral Tolerance occurs in

A

peripheral tissues

-spleen, lymph nodes, etc.

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19
Q

Mechanisms of Peripheral Tolerance for T cells

A

Suppression

Anergy

Deletion

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20
Q

Mechanisms of Peripheral Tolerance for B cells

A

Suppression

Anergy

Deletion

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21
Q

Positive selection occurs in the

A

cortex of thymus with assistance of cTECs (cortical epithelial cells)

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22
Q

Negative selection occurs in the

A

medulla of thymus with assistance of mTECs (medullary epithelial cells)

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23
Q

Type of cells that undergo positive selection in thymus

A

Double positive (CD4+/CD8+) thymocytes

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24
Q

Weak recognition of class II MHC + peptide

A

results in Mature CD4+ T cell

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25
Weak recognition of class I MHC + peptide
results in Mature CD8+ T cells
26
Strong recognition of either class I or class II MHC + peptide
results in apoptosis (negative selection)
27
T cells surviving negative selection
exist as Mature, Single Positive CD4+ or CD8+ T cells and leave the thymus
28
AIRE (Autoimmune Regulator Protein)
TF that resides in mTECs Controls expression of peripheral tissue self-antigens Critical role in negative selection and self-tolerance
29
Expression of air leads to
protective immunity
30
Deficiency of air leads to
Autoimmunity (APS-1 disease)
31
AIRE deficiency and regulatory T cells
Even in the absence of AIRE, you still get development of Tregs!
32
Central T lymphocyte Negative Selection
Deletion of immature lymphocytes that interact strongly with self antigen but, Imperfect Process
33
APECED
aka APS1 Autosomal recessive inheritance Mutations in AIRE gene (chromosome 21q22.3) Triad: "HAM"
34
APECED triad (symptoms)
"HAM" Mucocutaneous candidiasis Adrenal insufficiency Hypoparathyroidism
35
T cell Central Tolerance: Regulatory T cell Development
Some self-reactive CD4+ T cells will not be deleted, but instead will differentiate into regulatory T cells
36
Are all self-reactive T cells deleted following failure of Negative selection?
No, some self-reactive CD4+ T cells become Tregs
37
Development of Tregs is independent of
AIRE
38
Tregs exit thymus and enter the periphery in order to
inhibit responses against self-antigens
39
Important for inhibiting responses against self-antigens
Tregs
40
CD markers on Tregs
CD3+ CD4+ CD25 (high) and FoxP3+
41
Cytokines produced by Tregs
IL-10 and TGF-beta
42
Natural Tregs
made in thymus
43
APECED Clinical Manifestations
``` Candidiasis Hypoparathyroidism Adrenal failure Hypothyroidism DM Alopecia Vitilligo Gastritis/Pernicious anemia Immune hepatitis ```
44
Anergy defiintion
Functional unresponsiveness
45
Suppression definition
Block in activation
46
Deletion definition
apoptosis
47
Two signal hypothesis
-T cell proliferation and differentiation requires antigen-induced signals and costimulators
48
Best characterized pathway in T cell activation
B7: CD28 family of costimulators
49
CD28 expressed on
T cells
50
B7 expressed on
APCs
51
CTLA-4 expressed on
activated T cells and Tregs
52
CTLA-4 function
negative regulation of immune responses; self-tolerance
53
2 Mechanisms by which T cells become Anergic (unresponsive)
(1) block in signaling from TCR complex | (2) engagement of inhibitory receptors
54
2 Drugs involved in therapeutic manipulation of CTLA-4
Ipilimumab Abatacept
55
Ipilimumab
Monoclonal antibody against CTLA-4 enhances T cell activation and antitumor immunity
56
Abatacept
consists of EC domain of CTLA4 and Fc region of IgG1 binds CD80/86 (B7) on APC interrupts CD28-mediated costimulation causes T cell anergy
57
What cells do the drugs Ipilimumab and Abatacept bind?
Ipilimumab binds up T cells (binds at CTLA4) Abatacept binds up APCs (binds at CD80/86)
58
Tregs require ______ for growth
IL-2
59
CD25
receptor for IL-2
60
Tregs require _______ for function; expression is induced by ________
FoxP3 TGF-beta
61
3 Mechanisms by which Induced Peripheral T regs suppress immune responses
(1) Production of inhibitory cytokines (IL-10, TGF-beta) to inhibit effector T cell functions (2) Expression of CTLA-4 (to inhibit naive T cell activation) (3) Expression of IL-2 receptor and capture of IL-2
62
IPEX
mutations in FoxP3 gene X-linked recessive Triad: EDE
63
IPEX triad (symptoms)
EDE Enteropathy (diarrhea) Dermatitis (eczemous rash) Endocrine disease (diabetes/thyroid)
64
2 Mechanisms of Peripheral T cell Deletion (apoptosis)
(1) Deficiency of survival signals (expression of pro-apoptotic proteins induces apoptosis) (2) Engagement of death receptors (FasL binding Fas induces apoptosis)
65
Fas ligand expressed on
T cells
66
ALPS
disorder of apoptosis mutations in Fas, FasL, caspase 8/10 chronic accumulation of lymphoid cells defective lymphocyte apoptosis in vivo
67
ALPS symptoms
(1) Lymphoproliferation - splenomegaly - hepatomegaly - lymphadenopathy (2) Autoimmunity to RBCs - autoimmune hemolytic anemia - autoimmune thrombocytopenia - autoimmune neutropenia (3) Increased risk for lymphomas
68
B lymphocyte tolerance important for maintaining unresponsiveness to
(1) nonprotein, T-independent antigens (e.g. polysaccharides, lipids, nucleic acids) (2) protein self-antigens
69
Defective B lymphocyte tolerance may contribute to
autoantibody production in autoimmune disorders
70
In response to lipids, polysaccharides, etc. (non-protein antigens), B cells...
become (short-lived) IgM secreting plasma cells
71
2 responses to High-Avidity self-antigen recognition by Central B cells
(1) Receptor editing: expression of new Ig V region --> non-self reactive B cell (2) Apoptosis --> deletion
72
Response to Low-Avidity self-antigen recognition by Central B cells
(1) Reduced receptor expression, signaling --> anergic B cell
73
3 Mechanisms of Peripheral B Cell Tolerance in response to self-antigen binding
(1) Functional inactivation --> anergy (2) Apoptosis --> deletion (3) inhibitory receptors --> regulation/suppresion by inhib receptors
74
Failure of Self-tolerance results in
Self-reactive lymphocytes
75
Reaction to environmental stimuli in Autoimmunity
Environmental stimuli Tissue injury and inflammation Activation of tissue APCs Activation of self-reactive lymphocytes Self-reactive effector lymphocytes cause tissue injury: autoimmune disease
76
Single Gene Defects that cause autoimmunity
AIRE FOXP3 FAS
77
SLE
- Systemic autoimmune disorder (multi-organ) - Loss of immunological tolerance to multiple self antigens (defective B and T cell tolerance) - Autoantibodies primarily to nuclear constituents - Predominantly affects women of childbearing age
78
Genetic influences of SLE
family history complement deficiency (C1q, C2, C4) TREX1 HLA-DR2 and DR3
79
Antinuclear antibodies in SLE
Anti-dsDNA antibody Anti-Smith antibody
80
SLE symptoms
Malar rash Phostosensitivity Oral or nasal mucocutaneous ulcerations Nonerosive arthritis Nephritis Encephalopathy (seizures, psychosis)
81
Immunological self tolerance
unresponsiveness to specific antigenes INDUCED by exposure of lymphocytes to that antigen

IMM Exam 2 (15 decks)

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