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Immunology FirstAid > Immune Responses > Flashcards

Immune Responses Flashcards

1
Q

Immunoglobulin isotypes

A

Mature B lymphocytes express IgM and IgD on their surfaces. They may differentiate in germinal centers of lymph nodes by isotype switching (gene rearrangement; mediated by cytokines and CD40 ligand) into plasma cells that secrete IgA, IgE, or IgG.

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2
Q

IgG

A

Main antibody in 2° (delayed) response to an antigen. Most abundant isotype in serum. Fixes complement, crosses the placenta (provides infants with passive immunity), opsonizes bacteria, neutralizes bacterial toxins and viruses.

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3
Q

IgA

A

Prevents attachment of bacteria and viruses to mucous membranes; does not fix complement. Monomer (in circulation) or dimer (when secreted). Crosses epithelial cells by transcytosis. Most produced antibody overall, but released into secretions (tears, saliva, mucus) and early breast milk (known as colostrum). Picks up secretory component from epithelial cells before secretion.

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4
Q

IgM

A

Produced in the 1° (immediate) response to an antigen. Fixes complement but does not cross the placenta. Antigen receptor on the surface of B cells. Monomer on B cell or pentamer when secreted. Shape of pentamer allows it to efficiently trap free antigens out of tissue while humoral
response evolves.

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5
Q

IgD

A

Unclear function. Found on the surface of many B cells and in serum.

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6
Q

IgE

A

Binds mast cells and basophils; cross-links when exposed to allergen, mediating immediate (type I) hypersensitivity through release of inflammatory mediators such as histamine. Mediates immunity to worms by activating eosinophils. Lowest concentration in serum.

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7
Q

Thymus-independent antigens

A

Antigens lacking a peptide component (e.g., lipopolysaccharides from gram-negative bacteria);
cannot be presented by MHC to T cells. Weakly or nonimmunogenic; vaccines often require boosters (e.g., pneumococcal polysaccharide vaccine).

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8
Q

Thymus-dependent antigens

A

Antigens containing a protein component (e.g., diphtheria vaccine). Class switching and immunologic memory occur as a result of direct contact of B cells with Th cells (CD40–CD40 ligand interaction).

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9
Q

Acute-phase reactants

A

Factors whose serum concentrations change significantly in response to inflammation; produced by the liver in both acute and chronic inflammatory states.
Induced by IL-6, IL-1, TNF-α, and IFN-γ.

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10
Q

Positive (unregulated) acute0phase reactants

A

Serum amyloid A: Prolonged elevation can lead to amyloidosis.

C-reactive protein: Opsonin; fixes complement and facilitates phagocytosis. Measured clinically as a sign of ongoing inflammation.

Ferritin: Binds and sequesters iron to inhibit microbial iron scavenging.

Fibrinogen: Coagulation factor; promotes endothelial repair; correlates with ESR.

Hepcidin: Prevents release of iron bound by ferritin –> anemia of chronic disease.

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11
Q

Negative (down regulated) acute-phase reactants

A

Albumin: Reduction conserves amino acids for positive reactants.
Transferrin: Internalized by macrophages to sequester iron.

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12
Q

Complement - overview

A

System of interacting plasma proteins that play a role in innate immunity and inflammation. Membrane attack complex MAC defends against gram-negative bacteria.

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13
Q

Complement - activation

A

Classic pathway—IgG or IgM mediated.
Alternative pathway—microbe surface molecules.
Lectin pathway—mannose or other sugars on microbe surface.
“GM makes classic cars.”

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14
Q

Complement - functions

A 
C3b—opsonization.
C3a, C4a, C5a—anaphylaxis.
C5a—neutrophil chemotaxis.
C5b-9—cytolysis by membrane attack complex (MAC).
C3b binds bacteria.
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15
Q

Complement - opsonins

A

C3b and IgG are the two 1° opsonins in bacterial defense; C3b also helps clear immune complexes.

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16
Q

Complement - Inhibitors

A

Decay-accelerating factor (DAF, aka CD55) and C1 esterase inhibitor help prevent complement activation on self cells (e.g., RBC).

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17
Q

Complement disorders:

C1 esterase inhibitor deficiency

A

Causes hereditary angioedema.

ACE inhibitors are contraindicated.

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18
Q

Complement disorders:

C3 deficiency

A

Increases risk of severe, recurrent pyogenic sinus and respiratory tract infections; incr susceptibility to type III hypersensitivity reactions.

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19
Q

Complement disorders:

C5-C9 deficiency

A

Increase susceptibility to recurrent Neisseria bacteremia.

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20
Q

Complement disorders:

DAF (GPI anchored enzyme) deficiency

A

Causes complement-mediated lysis of RBCs and paroxysmal nocturnal hemoglobinuria.

21
Q

Complement disorders:

DAF (GPI anchored enzyme) deficiency

A

Causes complement-mediated lysis of RBCs and paroxysmal nocturnal hemoglobinuria.

22
Q

Cytokines secreted by macrophages:

IL-1

A

An endogenous pyrogen, also called osteoclast-activating factor. Causes fever, acute inflammation. Activates endothelium to express adhesion molecules; induces
chemokine secretion to recruit leukocytes.

“Hot T-bone stEAK”:
IL-1: fever (hot).
IL-2: stimulates T cells.
IL-3: stimulates bone marrow.
IL-4: stimulates IgE production.
IL-5: stimulates IgA production.
IL-6: stimulates aKute-phase protein production.
23
Q

Cytokines secreted by macrophages:

IL-6

A

An endogenous pyrogen. Also secreted by Th2 cells. Causes fever and stimulates production of acute-phase proteins.

“Hot T-bone stEAK”:
IL-1: fever (hot).
IL-2: stimulates T cells.
IL-3: stimulates bone marrow.
IL-4: stimulates IgE production.
IL-5: stimulates IgA production.
IL-6: stimulates aKute-phase protein production.
24
Q

Cytokines secreted by macrophages:

IL-8

A

Major chemotactic factor for neutrophils.
“Clean up on aisle 8.”
Neutrophils are recruited by IL-8 to clear infections.

25
Q

Cytokines secreted by macrophages:

IL-12

A

Induces differentiation of T cells into Th1 cells.
Activates NK cells.
Also secreted by B cells.

26
Q

Cytokines secreted by macrophages:

TNF-alpha

A

Mediates septic shock.
Activates endothelium.
Causes leukocyte recruitment, vascular leak.

27
Q

Cytokines secreted by all T cells:

IL-2

A

Stimulates growth of helper, cytotoxic, and regulatory T cells.

“Hot T-bone stEAK”:
IL-1: fever (hot).
IL-2: stimulates T cells.
IL-3: stimulates bone marrow.
IL-4: stimulates IgE production.
IL-5: stimulates IgA production.
IL-6: stimulates aKute-phase protein production.
28
Q

Cytokines secreted by all T cells:

IL-3

A

Supports the growth and differentiation of bone marrow stem cells. Functions like GM-CSF.

“Hot T-bone stEAK”:
IL-1: fever (hot).
IL-2: stimulates T cells.
IL-3: stimulates bone marrow.
IL-4: stimulates IgE production.
IL-5: stimulates IgA production.
IL-6: stimulates aKute-phase protein production.
29
Q

Cytokines secreted by Th1 cells:

interferon-gamma

A

Has antiviral and antitumor properties.
Activates NK cells to kill virus-infected cells,
Increases MHC expression and antigen presentation in all cells.

30
Q

Cytokines secreted by Th2 cells:

IL-4

A 
Induces differentiation into Th2 cells. 
Promotes growth of B cells. 
Enhances class switching to IgE and IgG.
“Hot T-bone stEAK”:
IL-1: fever (hot).
IL-2: stimulates T cells.
IL-3: stimulates bone marrow.
IL-4: stimulates IgE production.
IL-5: stimulates IgA production.
IL-6: stimulates aKute-phase protein production.
31
Q

Cytokines secreted by Th2 cells:

IL-5

A

Promotes differentiation of B cells.
Enhances class switching to IgA.
Stimulates the growth and differentiation of eosinophils.

“Hot T-bone stEAK”:
IL-1: fever (hot).
IL-2: stimulates T cells.
IL-3: stimulates bone marrow.
IL-4: stimulates IgE production.
IL-5: stimulates IgA production.
IL-6: stimulates aKute-phase protein production.
32
Q

Cytokines secreted by Th2 cells:

IL-10

A

Modulates inflammatory response. Inhibits actions of activated T cells and Th1. Also secreted by regulatory T cells.
TGF-β has similar actions to IL-10, because it is
involved in inhibiting inflammation.

33
Q

Cytokines secreted by Th2 cells:

IL-10

A

Modulates inflammatory response. Inhibits actions of activated T cells and Th1. Also secreted by regulatory T cells.
TGF-β has similar actions to IL-10, because it is
involved in inhibiting inflammation.

34
Q

Interferon alpha and beta

A

Interferes with viruses.
A part of innate host defense against both RNA and DNA viruses. Interferons are glycoproteins synthesized by viral-infected cells that act locally on uninfected cells,
“priming them” for viral defense. When a virus infects “primed” cells, viral dsRNA activates:
-RNAase L –> degradation of viral/host mRNA.
-Protein kinase –> inhibition of viral/host protein synthesis.
Essentially results in apoptosis, thereby interrupting viral amplification.

35
Q

Cell surface proteins

A

All cells except mature RBCs have MHC I.

36
Q

T cell surface proteins
(helper T cells)
(cytotoxic T cells)

A

TCR (binds antigen-MHC complex)
CD3 (associated with TCR for signal transduction)
CD28 (binds B7 on APC)

helper: CD4, CD40 ligand
cytotoxic: CD8

37
Q

B cell surface proteins

A

Ig (binds antigen)
CD19, CD20, CD21 (receptor for EBV), CD40 MHC II, B7

You can drink Beer at the Bar when you’re 21:
B cells, Epstein-Barr virus; CD-21.

38
Q

Macrophage surface proteins

A

CD14, CD40
MHC II, B7
Fc and C3b receptors (enhanced phagocytosis)

39
Q

NK cell surface proteins

A

CD16 (binds Fc of IgG), CD56 (unique marker for NK)

40
Q

Anergy

A

Self-reactive T cells become nonreactive without costimulatory molecule.
B cells also become anergic, but tolerance is less complete than in T cells.

41
Q

Effects of bacterial toxins

A 
Superantigens (S. pyogenes and S. aureus)—cross-link the β region of the T-cell receptor to the
MHC class II on APCs. Can activate any T cell, leading to massive release of cytokines.
Endotoxins/lipopolysaccharide (gram-negative bacteria)—directly stimulate macrophages by binding to endotoxin receptor CD14; Th cells are not involved.
42
Q

Effects of bacterial toxins

A 
Superantigens (S. pyogenes and S. aureus)—cross-link the β region of the T-cell receptor to the
MHC class II on APCs. Can activate any T cell, leading to massive release of cytokines.
Endotoxins/lipopolysaccharide (gram-negative bacteria)—directly stimulate macrophages by binding to endotoxin receptor CD14; Th cells are not involved.
43
Q

Antigenic variation

A

Classic examples:

  • Bacteria—Salmonella (2 flagellar variants), Borrelia (relapsing fever), Neisseria gonorrhoeae (pilus protein).
  • Virus—influenza (major = shift, minor =drift).
  • Parasites—trypanosomes (programmed rearrangement).

Some mechanisms for variation include DNA rearrangement and RNA segment reassortment (e.g., influenza major shift).

44
Q

Passive immunity

A

MEANS OF ACQUISITION Receiving preformed antibodies
ONSET Rapid
DURATION Short span of antibodies (half-life = 3 weeks)
EXAMPLES IgA in breast milk, maternal IgG crossing
placenta, antitoxin, humanized monoclonal antibody
NOTES After exposure to Tetanus toxin, Botulinum
toxin, HBV, or Rabies virus, patients are given preformed antibodies (passive)—“To Be Healed Rapidly”

45
Q

Active immunity

A

MEANS OF ACQUISITION Exposure to foreign antigens
ONSET Slow
DURATION Long-lasting protection (memory)
EXAMPLES Natural infection, vaccines, toxoid
NOTES Combined passive and active immunizations can be given for hepatitis B or rabies exposure.

46
Q

Vaccination

A

Vaccines are used to induce an active immune response (humoral and/or cellular) to specific pathogens.

47
Q

Live attenuated vaccine

A

Microorganism loses its pathogenicity but retains capacity for transient growth within inoculated host. Mainly induces a cellular response.

Pro: induces strong, often lifelong immunity.
Con: may revert to virulent form. Often contraindicated
in pregnancy and immune deficiency.

Exmples: Measles, mumps, rubella, polio (Sabin), influenza (intranasal), varicella, yellow fever.

48
Q

Inactivated or killed vaccine

A

Pathogen is inactivated by heat or chemicals; maintaining epitope structure on surface antigens is important for immune response. Humoral immunity induced.

Pro: stable and safer than live vaccines.
Con: weaker immune response; booster shots usually required.

Examples: Cholera, hepatitis A, polio (Salk), influenza (injection), rabies.

Immunology FirstAid (4 decks)

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