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Physiology Flashcards

1
Q

Mechanisms hypothesized to be involved in the breakdown of tolerance?
5

A
  1. Failure to delete autoreactive lymphocytes
    (Central tolerance failure and
    Peripheral tolerance failure)
  2. Molecular mimicry
  3. Abnormal presentation of self antigens
  4. Epitope spreading
  5. Polyclonal lymphocyte activation
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2
Q

What are epitopes?

A

the part of an antigen molecule to which an antibody attaches itself.

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3
Q

T cells

  1. Derived from where?
  2. Important in what process?
  3. Induce what to produce antigens?
  4. Each programmed to recognize what?
  5. Circulate in blood and sequestered in where? 2
A
  1. Derived from the thymus
  2. Important in cellular immunity
  3. Induce B cells to produce antigens
  4. Each programmed to recognize unique processed peptide fragment by T-cell receptor (TCR)
  5. Circulate in blood, sequestered in
    - spleen and
    - lymph nodes
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4
Q
  1. T cell activation: Which cells act as the antigen presenting cells? (APC)
  2. Major histocompatibility complex (MHC)— what is it?
  3. MHC—human leukocyte antigen (HLA). What are they?
  4. When NOT self peptide the APCs interact and present antigen to T-cells– which ones?
  5. Normal ratio?
A
  1. Dendritic cells and macrophages
  2. a region formed by genetic loci that plays a central role in humoral & cellular immunity
  3. group of proteins that participate in antigen presentation (APC)
  4. CD4 and CD8:
    CD4 T helper cells CD8 Cytotoxic T cells
  5. Normal ratio CD4/CD8—2:1
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5
Q
  1. CD4 and CD 8 expressing T cells are referred to as what?
  2. What do the helper T cells do?
  3. Describe what the Class I to III MHC molecules do?
    3
A
  1. CD4+ and CD8+
  2. The helper T cells—secrete cytokines & influence all other cells of the immune system
    • Class I MHC molecules—associated w/ recognition of endogenous antigens
    • Class II MHC molecules—associated w/ recognition of exogenous antigens
    • Class III MHC molecules—involved w/ the complement system
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6
Q

B LYMPHOCYTES

  1. Derived from where?
  2. Present where? 5
  3. After stimulation B cells form what?
  4. How many circulate?
A
  1. Derived from bone marrow
  2. Present in:
    - bone marrow,
    - lymph nodes,
    - spleen,
    - tonsils and
    - nonlymphoid organs such as GI tract (Peyers Patches)
  3. After stimulation B cells form plasma cells & secrete immunoglobulins
  4. 10-20% circulate
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7
Q 
IMMUNE SYSTEM REVIEW
Antigen processing:
1. Ag must be taken up by what?
2. Ag is then processed where?
3. Then it is presented to the what?
4. MHC class I/CD8+-- which cell?
5. MHC class II/CD4+-- which cell?
A
  1. APC
  2. inside the cell
  3. immune system
  4. cytotoxic cell
  5. helper T cell
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8
Q
  1. IMMUNOLOGICAL TOLERANCE is what?

2. It prevents the body from doing what?

A
  1. State of unresponsiveness specific for a particular antigen (Ag)
  2. It prevents the body from attacking itself—self-tolerance
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9
Q

B-Cell Tolerance:
1. Loss of self-tolerance with development of autoantibodies is characteristic of what?

Example:
2. Hyperthyroidism in Grave’s disease is due to what?

  1. Filtering autoreactive B-cells out of population. How? 4
A
  1. of a number of autoimmune disease
  2. autoantibodies to the thyroid-stimulating hormone receptors
    • Clonal deletion in bone marrow
    • Deletion of autoreactive cells in spleen or lymph nodes
    • Functional inactivation by anergy
    • Receptor editing- process that changes specificity of a B-cell receptor when autoantigen is encountered
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10
Q

T-Cell Tolerance:

Central mechanisms of T-cell tolerance involve the what?

A

deletion of self-reactive T-cells in thymus

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11
Q
  1. What is Positive Selection?

2. What is Negative Selection?

A
  1. Immature T cells of a clone that are not auto-reactive T cells are allowed to mature
  2. Immature T cell clones that have high affinity for host cells are sorted out and undergo apoptosis
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12
Q
  1. Many autoantigens are not present in thymus which results in what?
  2. Sequestered antigens (immunologically privileged) e.g.—Examples? 3
  3. Therefore, there needs to be what available to deal with these?
A
  1. self-reactive cells escaping the process
  2. -CNS,
    -eyes,
    -testes
    (if these are released then an immune response ensues)
  3. peripheral mechanism
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13
Q

Describe the Peripheral mechanism involved with T cell tolerance?
4

A

Peripheral activation of T-cells requires 2 signals:

  1. Recognition of peptide Ag with MHCs on the APCs AND
  2. Secondary costimulatory signals which are often absent
  3. Apoptosis (Fas receptor + Fas ligand)
  4. Suppressor T cells can also down-regulate autoreactive T-cells
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14
Q

Peripheral mechanism involved with T cell tolerance: Sometimes, no problem exists because what?

A

the self-reactive T-cells, remain immunologically ignorant because they can’t “see” Ag (Blood-brain barrier)

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15
Q

MECHANISM OF SELF-TOLERANCE

  1. What is central tolerance?
  2. What is peripheral tolerance? 2
  3. What is anergy?
A
  1. Central tolerance – Elimination of self-reactive T cells and B cells in the central lymphoid organs
  2. Peripheral tolerance :
    - Some of the T cells will become regulatory T cells (Tr)—products of Tr are cytokines that downregulate the immune response when the pathogen is cleared & help prevent autoimmunity
    - Some escaped T cells won’t recognize MHC-self-antigen and will remain as immature Tc cells
  3. “Anergy”= State of immunologic tolerance to Ag
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16
Q

MECHANISMS OF AUTOIMMUNITY: Much remains unknown but possibilities have been proposed: (5-7% of the population is affected by autoimmunity)?

4 possibilites

A
  1. Failure of mechanisms that maintain self-tolerance
  2. Genetic factors: genes that are involved in the immune response are the major players (MHC & HLA loci)
  3. Gender: autoimmune diseases affect females more severely and more often than men—hormonal influences play a role (estrogen)
  4. Infection & environmental factors: molecular mimicry*; environmental factors may contribute to or exacerbate (smoking)
17
Q

Autoimmune Disorders: Result from 1 or more mechanisms producing loss of self-tolerance. IN general this involves?

A

Immunologic cells are involved in tissue injury that results in exposure of self-antigen

18
Q

Possible mechanism of autoimmune dz?

A
  1. Failure of T-cell-mediated suppression
  2. Release of Sequestered Antigens
  3. Molecular Mimicry
  4. Heredity and Gender
19
Q

Possible mechanism of autoimmune dz: Failure of T-cell-mediated suppression: How does this occur? 2

A
  1. Failure to delete autoreactive immune cells

2. Increasing ratio of CD4 to CD8 may be involved

20
Q

Possible mechanism of autoimmune dz: Release of Sequestered Antigens? 2

Example?

A
  1. Normally body does not produce Ab against self Ag
  2. Any self Ag sequestered from immune system during development and then reintroduced is considered foreign

Examples: Sperm and ocular Ag following post-traumatic uveitis and orchitis following vasectomy

21
Q

Describe Molecular Mimicry? 2

Examples? 2
describe the PP in these examples

A
  1. Molecular Mimicry:
    - Foreign Ag so closely resembles a self Ag that Ab produced against former attack the later
    - B-cell or T-cell response can be mounted against antigentically altered or injured tissue creating an immune response
  2. EXAMPLES:
    -Rheumatic Fever and
    -Acute Glomerulonephritis:
    (A protein in the cell wall of group A Beta hemolytic streptococci has considerable similarity to Ag in heart and kidney)
22
Q

Autoimmune: POSSIBLE mechanisms (Continued)

  1. Describe Hereditary and Gender mechanism of action?
    - Example?
  2. The exact trigger that causes the autoimmune disease in patients with certain HLA types is unknown although there are some possible theories? 3
A
    • Certain inherited HLA types occur more frequently with certain immunological disorders
    • Example: 90% of patient with ankylosing spondylitis carry the HLA-B27 Ag
    • Certain viral or bacterial infections
    • Chemical substance exposure
    • Self Ag that has been hidden from immune system during development becomes released
23
Q

Almost all autoimmune diseases are more common in women, therefore what may play a big role?

24
Q

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)‏

  1. Genes?
  2. More common in who? 2
  3. Produce autoantibody to what?
  4. What can be affected?
A
  1. HLA DR2 and DR3
  2. -85% of patients are female & More common in blacks (1:250) versus whites (1:1000)
    -Strong familial link:
    If mother has SLE then daughter with 1:40 chance and son 1:250 chance
  3. Produce autoantibodies to nuclear Ag
  4. Multiple organ systems are affected
25
Q

SLE PATHOGENESIS
1. Many effects are secondary to trapping what?

  1. Other effects are autoantibody mediated destruction of what?
A
  1. Ag-Ab complexes in capillaries of visceral structures

2. host cells (thrombocytopenia)

26
Q

SLE ENVIRONMENTAL FACTORS
1. Estrogen stimulates what? 5

  1. Estrogen increases macrophage proto-oncogene expression and reduces what?
  2. What are immunosuppressive?
  3. What affect immunoreactivity and favor autoantibody production? 2
A
    • T cells,
    • B cells,
    • macrophages,
    • releases some cytokines, &
    • cell adhesion molecules
  2. apoptosis in self-reactive B cells
  3. Androgens
  4. Progesterone and prolactin
27
Q

Other SLE ENVIRONMENTAL FACTORS? 3

A
  1. UV light exacerbates the disease
  2. Viruses can stimulate specific cells in the immune network:
  3. Some drugs can cause lupus-like syndromes:
28
Q
  1. SLE flares can follow what?
  2. SLE pts have higher titers of what?
  3. What are two drugs that often cause lupus-like syndorme?
A
  1. Lupus flares may follow bacterial infections
  2. Patients w/ SLE have higher titers to EBV
    • Procainamide
    • Hydralazine
29
Q

RHEUMATOID ARTHRITIS (RA)

  1. Associated with what genes?
  2. Disease initiated how?
  3. Target is what?
  4. Autoantibodies are produced against what? 4
A
  1. Genetic predisposition—associated with HLA-DR4 and/or HLA-DR1
  2. Disease in initiated by activation of helper T cells responding to some arthritogenic agent (possibly microbial)‏
  3. Target is the synovial lining of joints
  4. Autoantibodies are produced against:
    - Type II cartilage,
    - Cartilage antigenic glycoprotein-39,
    - Immunglobulin G,
    - Citrullinated proteins and peptides
30
Q

RA SYNOVITIS
1. Angiogenic cytokines stimulate growth of what?

  1. Results in what into joint?
  2. What activate endothelial cells—produce adhesion molecules? 2
  3. Together with transmigration of lymphocytes; PMNs enter where?
  4. Activated CD4+ cells:
    Do what? 2
A
  1. new blood vessels
  2. transudation of fluid
    • Tumor necrosis factor (TNF) &
    • substance P
  4. synovial space
    • Activate macrophages and other cells
    • Activate B cells producing Abs
31
Q

IMMUNE RESPONSE IN SYNOVIUM
1. Rheumatoid synovium has both what derived cytokines? 2

  1. Cytokines (IL-1 and TGF-alpha) also cause what? 2
  2. Activated rheumatoid synovium eventually destroys what? 2
  3. Simultaneously osteoclasts and osteoblasts are activated by synovial cytokines destroying what?
A
  1. lymphocyte and macrophage
  2. synovial and chondrocyte proliferation
  3. cartilage and tendons
  4. subchondral bone
32
Q

RHEUMATOID FACTOR
1. 70% of patientss w/ RA are what?

  1. What are generated that are directed against the Fx portions of IgG?
  2. RF and IgG form immune complexes that do what? 2 and lead to?
  3. Circulating RF contributes to the what of RA? 2
A
  1. RF+
  2. Autoantibodies (IgM and some IgG)
    • fix complement, attract neutrophils and
    • lead to tissue injury
    • extra-articular manifestations of RA and
    • the synovial inflammation
33
Q
  1. What is scleroderma?
  2. What do the autoantibodies in this stimulate? Causing?
  3. Which decades?
  4. Women or men?
  5. Two types? 2
A
  1. Diffuse fibrosis of skin and internal organs
  2. platelet derived growth factor receptors (PSGFR) causing fibroblast dysregulation
  3. 3rd through 5th decade
  4. 3 times more common in women than men
  5. Two types: Limited (80%) and Diffuse (20%)
34
Q

LIMITED SCLERODERMA
1. 80% of cases—limited to where? 2

  1. What is CREST Syndrome? 5
A
  1. face and hands
    • Calcinosis cutis
    • Raynaud’s phenomenon
    • Esophageal motility disorder
    • Sclerodactyly
    • Telangectasias
35
Q

DIFFUSE SCLERODERMA

  1. What percent of cases?
  2. Main characteristic?
  3. Organ involvement of ?2
  4. More or less severe that limited?
A
  1. 20% of cases
  2. Tendon friction rubs over wrists, ankles, and knees
  3. Lung and cardiac involvement
  4. The more severe form

Rheumatology (11 decks)

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