Immune System Overview Flashcards

1
Q

Adaptive Immunity

A
  • Aquired
  • Specific recognition of small portion of organism or triggering antigen, Specific response to infectious agent
  • Generate memory of initiator
  • Should eliminate self-reacting cells
  • Two types: Humoral and Cell-mediated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Innate Immunity

A
  • Natural
  • First line of defense
  • No previous exposure to antigen required
  • Nonspecific: Physical and chemical mechanical barriers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Natural Killer Cells

A
  • 10-15% of total lymphocytes
  • Destroy virus-infected and tumor cells
  • Lack antigen specificity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Mast Cells

A

Inflammatory cells, in tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Antigen Presenting Cells (APC)

A
  • Dendritic cells
  • Macrophages
  • B cells
  • Have MHC Class 2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Epitope

A
  • Specific site on the antigen to which antibody or T cell receptors bind
  • One antigen can have many epitopes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Antibody Structure

A
  • Each monomer of antibody - “Y” shaped
  • 2 heavy chains: give antibody its name
  • 2 light chains: both kappa or both lambda
  • Each monomer has 2 Fab (antibody- binding) regions Each Fab contains 1 heavy and 1 light chain
  • Each monomer has 1 Fc (crystallizable) containing 2 heavy chains
  • Complement fixation occurs at Fc region
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Secondary Lymphoid Organs

A

Lymph nodes, spleen, Peyer’s patches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Primary Immune Response

A

IgM antibody appears first, followed by IgG on first exposure to antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Secondary Immune Response

A
  • Follows re-exposure to the same antigen
  • Shorter response time
  • Larger quantity of IgG
  • Persists longer due to memory cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Active Immunity

A
  • Infection/exposure to antigen (natural)
  • Vaccination (artificial)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Passive Immunity

A
  • Igs crossing placenta
  • Abs secreted in breast milk
  • Injections of gammaglobulins and Abs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Adoptive Immunity

A
  • Anti-cancer treatment
  • Introduction of natural killer cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Forbidden Clone

A

Self-reactive clone of lymphocytes not destroyed, the immune response to self-antigens could cause disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Sequestered Antigen

A

Antigens (eye lens, sperms) not normally in contact with the immune system get released (trauma, surgery etc.), and hence won’t be recognized as self-antigens.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Immunologic Deficiency

A

With aging, suppressor T lymphocytes decrease and no longer control T helper/B lymphocyte interactions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Features of Autoimmune Disease

A
  • Most autoimmune diseases are chronic
  • Significant morbidity and mortality result
  • Women more frequently affected
  • Mostly in adults between 20-40 yrs of age
  • Some diseases cause initial tissue damage; others do not
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Beneficial Autoantibodies

A

CD5 cells produce autoantibodies to clear dead cells and remove damaged cellular components.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Central Tolerance

A
  • Initiated during fetal development
  • Eliminates cells with potential to react strongly with self-antigens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Peripheral Tolerance

A
  • Occurs in the circulation
  • Process involves mature lymphocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Factors Causing Loss of Tolerance

A
  • Genetic
  • Hormonal
  • Environmental
  • Failure of a regulatory sequence in the immune response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Mechanisms for Developing Autoimmunity

A
  • Molecular mimicry and cross-reactivity
  • Alteration of self-antigens
  • Trauma exposing sequestered antigens
  • Polyclonal activation of self-reactive lymphocytes
  • Altered expression of MHC receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Effector Mechanism Classification

A

(underlying initiator) Initiator of damage: Autoantibody T cells - Cytokines released by lymphocytes can add to the tissue damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Organ or System Attacked Classification

A

Organ-specific: damage is to a single organ

Example: Hashimoto’s thyroiditis

Systemic: autoantibodies cause damage in multiple organ systems

Example: systemic lupus erythematosus (SLE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

B cell Maturation

A
  1. Undifferentiated stem cell in bone marrow
  2. Progenitor (Pro-B) cell – CD45R on membrane, DNA rearrangement
  3. Pre-B cell – IL-7 receptor on cell surface
  4. Mature B cell (virgin B cell)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

IL-4

A
  • Promotes vigorous proliferation of the activated B cell
  • Up-regulates B cell production of MHC Class II
27
Q

IL-5

A
  • Stimulates proliferation of activated B cells
  • Stimulates differentiation of B cells into plasma and memory cells
28
Q

IL-6

A

Stimulates differentiation of activated B cells into plasma cells

29
Q

Memory B cell Characteristics

A

Express high levels of complement receptors and adhesion molecule

30
Q

Isotype

A
  • Portion of constant region of heavy chain that differs between Ig classes and subclasses
  • Portion of constant region of light chains
31
Q

Allotype

A

Variation of alternative alleles at a single gene locus

32
Q

Idiotype

A
  • Part of hyper variable regions of antibody (ab) molecule
  • Unique to abs produced by single clone of B cells
33
Q

IgG

A
  • 80% of total human immunoglobulin
  • Monomer (2 heavy and 2 light chains)
  • Responsible for long-term immunity
  • Only Ig able to cross placenta
  • Activates classical complement pathway
  • Has 4 subclasses, each with different biological activity
34
Q

IgA

A
  • 10-15% of total immunoglobulin
  • 2 subclasses:
  1. Serum IgA: usually a monomer
  2. Secretory IgA: dimer or tetramer with secretory piece, allowing IgA to resist proteolysis
  • Secretory IgA is the predominant Ig in secretions: mucous membranes, saliva, tears
35
Q

IgM

A
  • 5-10% of total serum immunoglobulin
  • Pentamer joined by a J chain
  • First Ig produced in the immune response
  • Can be found in low concentrations in secretions
  • Effective activator (due to size) of the classical complement pathway
36
Q

IgD

A
  • 0.2% of total serum immunoglobulin
  • Monomer
  • Most IgD is membrane-bound to mature B cells
37
Q

IgE

A
  • Less than 0.002% of total serum Ig
  • Binds to mast cells and basophils at Fc
  • Fab binds allergen and causes degranulation of these cells: Histamine release initiates allergic response
  • Provides immune response to parasites
38
Q

Complement System

A
  • Works with antibody to defend against bacterial infection
  • Aids in antigen presentation
  • Causes organism lysis
39
Q

General features Of Complement System

A
  • Most abundant component is C3
  • Helps in getting rid of immune complexes and inflammatory products
  • Complement fragments are opsonins, chemotactic agents, and anaphylatoxins
  • Complement system is linked to the coagulation, fibrinolytic, and kinin cascades
40
Q

Complement Factor Creation

A
  • Most components manufactured in liver
  • C1 comes from intestinal epithelial cells or activated macrophages
  • Factor D made in adipose tissue
41
Q

Classical Pathway

A

An antigen/antibody reaction is required to activate the pathway (1 molecule of IgM or 2 closely associated molecules of IgG)

  1. Recognition: C1q, C1r, C1s
  2. Activation: C4, C2, C3
  3. Membrane attack complex (MAC): C5-C9
42
Q

MAC

A
  • Involves C5-C9
  • Activated C4b2a3b cleaves C5 – begins final stage of the complement cascade
  • C5 cleaved to C5a (a potent anaphylatoxin) and C5b (binding molecule for C6-C9)
  • C6 and C7 deposited on cell membrane; lysis begins with the addition of C8 (a channel is formed in the cell membrane– Potassium leaks out of cell)
  • C8 binds multiple C9 molecules, completing the channel – Sodium, calcium, and water enter the cell, causing lysis
43
Q

Alternate Pathway

A
  • Not activated by antibody but by cell walls of bacteria, fungi, viruses, and some parasites
  • Factor D: similar function to C1qrs
  • Factor B: similar to C2
  • Properdin: stabilizing molecule
  • Once C3 is cleaved, process for forming MAC is identical to classical pathway
44
Q

MBL

A
  • Part of innate immune system
  • Functions early in bacterial infection
  • May be important in children aged 6-18 months; the time between decrease in maternal antibody and full development of child’s adaptive immune system
  • Carbohydrates that bind to MBL:
  1. Mannose
  2. n-acetylglucosamine
  3. fucose
  4. glucose
45
Q

Total Hemolytic Complement (CH50) Assay

A
  • Screening test for function of classical pathway:
  • Based on ability of patient’s complement to lyse a standardized amount of antibody-coated sheep RBCs
  • CH50 low if any factor is deficient
  • Value is “zero” in total lack of complement
  • CH50 value: dilution that lyses 50% RBCs
46
Q

AH50 Assay

A
  • Screening test for alternate pathway function:
  • Rabbit blood cells (can activate alternate pathway) used instead of sheep RBCs
  • Sequence of factors D, B, P, and C5-C9 are evaluated
  • If both CH50 and AH50 are abnormal, defectisin C3 or C5 through C9
  • If only CH50 is abnormal, defect is in C1, C4, or C2
47
Q

Sensitivity

A

The proportion of individuals with the disease who test positively with the test

High sensitivity = few false negatives

48
Q

Specificity

A

The proportion of individuals without the disease who test negatively for the disease

High specificity = few false positives

49
Q

Titer

A

Determination of antibody levels that change during acute and convalescence phases. Best approach to diagnosis an acute infection is the presence of specific IgM tests vs. detection of IgG during convalescence.

50
Q

Prozone Readings

A

If titer reads initially negative in preliminary tubes, then becomes positive, the antibody has been sufficiently diluted to allow the Ag/Ab complex to form. –These dilutions are @ zone of equivalence.

51
Q

Antigen/Antibody Detection Tests

A
  • Precipitation tests: followed by electrophoresis Agglutination tests:
  • Latex agglutination
  • Hemagglutination
  • Inhibition reactions Complement fixation tests
  • Immunoassays and labeling techniques
  • Molecular diagnostics assays
52
Q

Common Dysproteinemias

A

Multiple myeloma: Neoplastic proleferation of single clone of plasma cells. These produce a specific type of gamma globulin

Waldenstrom’s Macroglobulinemia: Plasma cell proliferation disorder malignant lymphocytes produced

53
Q

Primary versus Secondary Response (Ig)

A
54
Q

Anamnestic Response

A

Secondary response with high levels of IgG, after a second exposure to an antigen that created memory cells

55
Q

Factors the influence Ab-Ag reactions (4)

A
  1. pH
  2. Concentration of Reactants
  3. Length of incubation
  4. Temperature
56
Q

Hapten

A

A low molecular weight molecule that is too small to generate an immune response alone; needs and adjuvant

57
Q

Classical Pathway

A

Triggered by Ab

  1. C1
  2. C4/C2/C3
  3. C5-C9
58
Q

Alternative Pathway

A

Triggered by lipoproteins found in bacterial walls

  1. C3b
  2. Bb
  3. P
  4. Form C3bBb3bP/C5-C9
59
Q

Heterophile Ag

A

Heteroantigens that exist in unrelated plants and animals that are nearly identical and can cause cross-reactivity

60
Q

Heterophile Ab

A

Stimulated by one Ag but can react with an unrelated surface Ag present on other cells

61
Q

Forssman Ag

A

An Ag found in certain animals and pneumococci that are not Paul-Bunnell Ag

62
Q

Forssman Ab

A

A heterophile Ab not related to IM that causes hemagglutination

63
Q

Interpreting Paul-Bunnell Test Results

A

If agglutination occurs, the IM was caused by EBV

64
Q

MonoSpot test Principle

A

Agglutination of horse RBCs with Paul-Bunnell Ag that will only agglutinate in the presence of anti-Paul-Bunnell IgG