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Immunology > Immunity mediated by B cells and antibodies > Flashcards

Immunity mediated by B cells and antibodies Flashcards

1
Q

Events that occur in the 1st week of the primary immune response

A
  • B cell activation: Signal 1 and 2
  • Short lived plasma cells secreting IgM
  • Primary focus for expansion of antigen activated B cells is in the medullary cords
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2
Q

Events that occur in the 2nd week of the primary immune response

A

Formation of germinal centers

  • isotype switching
  • somatic hypermutation
  • development of memory B cells and long lived plasma cells (expansion of antigen-activated B cells in the primary follicle creates the germinal center)
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3
Q

Different types of B cells

A
  • Mature naive B cells
  • Marginal zone B cells
  • B-1 B cells
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4
Q

Effector functions of antibodies

A
  • IgM: protects bloodstream
  • IgG: protects bloodstream, extracellular spaces, lymphatics
  • IgA: 1st line of defense, present in mucous secretions and protects epithelial surfaces
  • IgE: 2nd line of defense, stimulates an inflammatory response
  • IgD: participates as a BCR on naive B cells
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5
Q

Events that occur in week 1

A
  • recognition of antigen
  • activation by helper T cells and formation of a primary focus
  • differentiation to short lived plasma cells that produce IgM to clear the infection
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6
Q

Primary focus

A

A pool of B cells resulting from the proliferation of antigen activated B cells over the course of 3-4 days

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7
Q

Events that occur in week 2

A

Steps to pathogen-specific memory formation occur

  • development of antibodies with a new heavy chain isotope (IgA,G, or E) and with a higher affinity for epitopes derived from original pathogen
  • development of long-lived plasma cells
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8
Q

Signal 1

A

Recognition of antigen

- prepares B cells for collaboration with effector helper T cells

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9
Q

Signal 2

A

Activation by effector helper T cells

  • formation of a primary focus
  • must happen within the first 24 hours or cell will undergo apoptosis
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10
Q

What happens to B cells in the first week?

A
  • Some activated B cells differentiate to short-lived plasma cells secreting IgM
  • Other activated B cells in the primary focus will participate in the events that take place in the 2nd week of the primary immune response
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11
Q

Germinal center

A

Site of B cell proliferation in the B cell area of secondary lymphoid tissues

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12
Q

Changes in _______ expression is responsible for the interaction of antigen-activated B cells with effector helper T cells

A

Chemokine receptor

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13
Q

____ and ____ induce B cell to migrate into T cell area

A

CXCR5 and CCR7

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14
Q

B cell and T cell migration

A

Antigen activated B cells migrate to T cell area, and antigen activated helper T cells migrate to B cells
- form a conjugate and synapse so signal 2 is secreted directly on the B cell surface (eliminates bystander effects)

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15
Q

Function of germinal centers

A
  • isotype switching
  • somatic hypermutation
  • development of memory B cells and long lived plasma cells
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16
Q

Isotype switching

A

Efficient elimination of the pathogen
- germinal center B cells undergo isotype switching from IgM to an isotype that is most effective in removing the pathogen

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17
Q

Somatic hypermutation

A

Efficient recognition of the pathogen

  • point mutations are generated in the variable region of the heavy chain and light chain genes
  • B cells in the germinal center are then selected for high affinity recognition of the original antigen epitope
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18
Q

Protection from reinfection and disease

A

Germinal center B cells will differentiate into either antibody secreting long lived plasma cells or memory B cells

  • long lived plasma cells migrate to the bone marrow and secrete higher affinity and isotype switched antibody that is observed during the later part of primary response
  • memory B cells maintain surveillance of secondary lymphoid tissues
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19
Q

Events in the _____ will determine life span of B cells once plasma cell has exited the bone marrow

A

Germinal center

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20
Q

What characteristics of the antibody response will be helpful in preventing disease

A
  • antibody response occurs more rapidly (3-5 days)
  • antibody levels will be higher than the level attained with the primary response
  • antibodies produced will have a higher affinity for the antigen epitope
  • antibody will consist of an isotype different from IgM
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21
Q

2 types of antigens encountered by B cells

A

Thymus dependent protein antigens
- requires T cell help - signal 2

Thymus independent non protein antigens
- antigen provides both signals

22
Q

Thymus dependent antigen

A

Protein antigens require T cell help for B cell proliferation and differentiation

23
Q

Thymus independent antigen

A

Polysaccharides from bacterial capsules and some viruses (antigen can provide both signal 1 and 2)

  • repeated epitopes of these antigens can engage BCRs and TLRs
  • multitude of signals is sufficient to induce B cell proliferation and differentiation to short lived plasma cells secreting IgM = early IgM response to infection
24
Q

B cells recognize ___ and T cells recognize ___

A

Polysaccharide; protein portion of an antigen

25
Q

Follicular B cells

A

Aka: mature naive B cells

  • adaptive immunity
  • diverse repertoire of antibody specificities that respond to thymus-dependent antigens
  • require T cell help for activation (signal 2)
  • location: secondary lymphoid tissues, recirculate between the blood and lymphatics
26
Q

Marginal zone B cells

A

Respond to pathogens in the blood

  • differentiate to short lived plasma cells secreting IgM
  • location: marginal zone of the spleen where the blood is filtered
27
Q

B-1 B cells

A

Respond to pathogens entering the major body cavities

  • differentiate to short lived plasma cells secreting IgM
  • location: peritoneal and pleural cavities
28
Q

Why do we have different antibody isotypes?

A

We need different antibody effector functions because of different kinds of pathogens.
We also need to protect the different body compartments where pathogens invade

29
Q

In what general ways do antibodies clear infections with extracellular pathogens and their products?

A

Focus defense mechanisms onto the pathogen itself

- antibody links the pathogen with the leukocytes and plasma proteins that will eliminate it

30
Q

Effector functions of antibodies

A
  • neutralization
  • opsonization: phagocytes express Fc receptors for antibody bound to a pathogen
  • activation of complement: phagocytes express complement receptors for C3b bound to a pathogen
31
Q

Fc region

A

C terminus of antibody is also called Fc region

  • Fc receptors for IgG, IgA, and IgM
  • low affinity: cannot bind to free IgG or antibody from the plasma
32
Q

IgM

A

Is confined to the bloodstream, but does enter tissue at a site of infection
- is not recognized by Fc receptors of phagocytes, but phagocytes express receptors for complement component C3b that is deposited onto surface of the pathogen

33
Q

How does IgM clear an infection?

A

IgM is a potent activator of complement and is specialized to activate complement efficiently upon binding to the pathogen

34
Q

C1q

A

First component of the classical complement pathway, must bind two or more antibody heavy chains to become activated –> requires multiple molecules of IgG bound to the pathogen
- a single molecule of IgM bound to the pathogen is sufficient for activation of complement due to pentameric structure of IgM

35
Q

Effector function of IgG

A

Neutralization!
- prevents infection of cells by neutralizing bacterial and viral toxins
Opsonization!
- macrophages and neutrophils express Fc receptors for IgG
Antibody-dependent cell mediated cytotoxicity!

36
Q

What is neutralization?

A

Antibodies can prevent infection by coating the surface of a pathogen and prevent the pathogen from binding to healthy cells

37
Q

What is an opsonin?

A

A substance that enhances phagocytosis

- ex: IgG

38
Q

Antibody dependent cell mediated cytotoxicity

A

Natural killer cells express Fc receptors for IgG

- NK cells use their Fc receptors to bind to antibody coated cells, which they kill by inducing apoptosis

39
Q

Antibody-coated cells recognized by NK cells

A
  • virus infected cells

- tumor cells

40
Q

IgA

A

Formed after a primary response to a pathogen in the respiratory tract or upper intestinal tract
- germinal centers that form in the 2nd week of the response will produce memory B cells that have IgA as an antigen receptor and long-lived plasma cells which will secrete IgA

41
Q

How does IgA provide the first line of defense against re-infection?

A

IgA is present in mucus secretions that cover the epithelial linings of the body

42
Q

How does IgA protect the epithelial surfaces?

A

Neutralization

43
Q

Does IgA activate complement?

A

No, IgA is a dimer that is unable to activate complement

44
Q

Should complement be activated at epithelial surfaces?

A

No! Will result in tissue damage at intestinal surfaces due to cytokine storm, reason why you need an antibody potent in neutralization (IgA)

45
Q

Migration of IgA to epithelial surface

A

Binding of IgA to receptor on basolateral face of epithelial cell –> receptor mediated endocytosis of IgA –> transport of IgA to apical face of epithelial cell –> receptor is cleaved, IgA is bound to mucus through the secretory piece

46
Q

IgE

A

Second line of defense, behind IgA

  • primary response to parasites results in long-lived plasma cells secreting IgE
  • mast cells stimulate an anti-parasitic response –> IgE provides mast cells the ability to “sense” pathogens
47
Q

Mast Cells

A
  • located beneath the epithelial surfaces of the skin, respiratory tract, and GIT
  • express Fc-receptors for IgE (high affinity, can bind free IgE that is not bound to an antigen)
  • when an antigen binds IgE on the surface of mast cells = release of histamine stimulates an inflammatory response
48
Q

Mast cells are found in ____ and respond to _____

A

tissues; parasite infection

49
Q

Mast cell activation

A

Inflammation at the site of infection

  • histamine: vascular permeability, peristalsis
  • TNF alpha: vascular permeability, upregulation of cytokines
50
Q

How does IgE provide a second line of defense against re-infection with pathogens that invade the intestinal epithelium and enter the underlying tissue?

A

IgE is bound to the surface of mast cells and is responsible for mast cell activation in response to pathogen invasion

51
Q

Eosinophils

A

Express Fc receptors for IgE

  • binding to IgE coated pathogen induces degranulation, release proteins that damage larvae membrane
  • type of antibody-dependent cellular cytotoxicity

Immunology (28 decks)

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