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BIO 320 Immunology > Lecture 7 Continued for Individual Exam 3 > Flashcards

Lecture 7 Continued for Individual Exam 3 Flashcards

1
Q

What Ig’s are naturally expressed in BCRs?

A

Monomeric IgD (Cδ) and IgM (Cµ)

  • expressed naturally in the constant region of the BCR
  • 2 antigen binding sites
  • transmembrane anchor
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2
Q

What is Igα/Igβ?

A

Responsible for intracellular signalling for B cell activation

-similar to the CD3 complex on T Cells

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3
Q

What kinds of antigens can BCRs and TCRs bind?

A

BCR = Native Antigen

TCR = Processed Antigen

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4
Q

What is TD B Cell activation?

A

Thymus Dependent

-Requires TH help for B Cell activation

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5
Q

What are the steps of Thymus Dependent B Cell Activation?

A

1a. Exogenous antigen binds BCR

-entire antigen is endocytosed, processed, loaded on MHC II

1b. Peptides presented with MHC II to TH

-Intracellular signalling with Igα/Igβ in B cell

2. Co-stimulation by CD40/CD40L

-CD40L on TH binds CD40 on B Cell = more intracellular signals

3. Cytokine stimulation by TH

  • TH recognizes same antigen as B cell and releases cytokines
  • The type of TH it binds results in different cytokines being released by TH
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6
Q

What does presentation to a TH always result in?

A

Cytokine signalling

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7
Q

What is activated by presentation by the various APCs?

A

Dendritic Cells and Macrophages

-present to T cell to active that T cell

B Cells

-present to T cell to activate itself

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8
Q

What can a B cell differentiate into with and without presentation to a TH cell?

A

Thymus Dependent (TD)

  • TH1 ⇒ IFγ ⇒ B Cell ⇒ Plasma Cell ⇒ IgG
  • TH2⇒ IL-5⇒ B Cell ⇒ Plasma Cell ⇒ IgE or IgA

Thymus Independent-1 (TI-1)/Thymus Independent-2 (TI-2)

  • no cytokine signalling
  • B Cell ⇒ Plasma Cell ⇒ IgM or IgD
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9
Q

What are the steps of thymus independent-1 B cell activation?

A

1. Antigen (e.g. LPS) binds BCR

-1st intracellular signal

2. Antigen binds TLR (e.g. TLR4) on same cell

-2nd intracellular signal

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10
Q

What are the steps of thymus independent-2 B cell activation?

A

1. CD21 and BCR are cross-linked by bacterium opsonized by C3d

  • Antigen binds BCR
  • Antigen has been opsonized with C3d
  • C3d binds to CD21 on B cell
  • 2 signals= 1 from BCR binding and one from CD21 binding

OR

1. Antigen with repetitive epitopes (e.g. capsular polysaccharides) cross-links multiple BCRs

  • One BIG signal from the repetitive epitopes on antigen
  • Repetitive epitopes are additive
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11
Q

After activation and clonal expansion occurs, what happens next to the B cell and where does this occur?

A

Activation occurs in the T cell zone

The activated B cell moves to the geminal center where Affinity selection and Class switching occurs

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12
Q

What is affinity selection and class switching?

A

Affinity selection

  • somatic hypermutation and affinity selection
  • antigen fits in the antigen binding site due to VDJ recombination
  • mutations in the VDJ region to make antigen bind better

Class switching

  • changes in the constant region of antibody
  • changes class of antibody to correct type to fight infection
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13
Q

What is somatic hypermutation?

A

Random point mutations are created in the V region

  • AID: activation-induced cytifine deaminase
  • gene involved in somatic hypermutation that causes mutations
  • does not affect specificity of Ag binding
  • affects affinity of Ag binding
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14
Q

What is affinity selection?

A

After somatic hypermutation the new BCRs are tested for binding

  • follicular dendritic cell (FDC) presents same antigen
  • must receive positive signal from FDC to survive
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15
Q

What is class switch recombination?

A

Determines isotype of immunoglobulin produced by plasma cells

-AID cuts out CX regions we don’t want then splices in remainder to change class

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16
Q

What happens to the B cells after affinity selection and class switching?

A

Once the infection is over some of these new B cells are kept as memory cells

-improves 2nd response

The process is repeated to continuously refine the B Cells and make them better

17
Q

What is class switching influenced by? What would happen if we had a TH defect?

A

Class switching is influenced by cytokines and CD40 ligand co-stimulation

  • If there is a mutation in the TH cell, especially CD40/CD40L, it will prevent class switching
  • No class switching means only IgM and IgD produced
  • Leads to X-Linked HIGM = Immunodeficiency/infection prone
18
Q

What does the following graph tell you?

A

During primary response

  • innate immunity important and holds the line during latent period
  • IgM initially produced and then as IgG starts being produced IgM declines

During secondary response

  • much faster almost no latent period
  • IgG produced immediately
  • IgM produced more slowly
19
Q

What are the functional differences between Naive and Memory B cells for

  • Magnitude of peak antibody resposne
  • antibody isotype produced
  • antigens
  • antibody affinity
  • lifespan
A

Magnitude of peak antibody response

  • Naive: varies
  • Memory: 10-100x higher than naive

antibody isotype produced

  • Naive: IgM during early primary response
  • Memory: IgG predominates, except in mucosal tissue=IgA

antigens

  • Naive: TD and TI-1, TI-2
  • Memory: TD

antibody affinity

  • Naive: low
  • Memory: high

lifespan

  • Naive: short lived
  • Memory: long lived
20
Q

How does IgM and IgG help fight infection?

A

IgM - complement activation

IgG - opsonization and complement activation

-increased affinity too

21
Q

What is antibody-mediated (humoral) immunity?

A

Plasma cells produce antibodies that specifically bind to microbial antigens which leads to clearance

  • B Cells activated⇒Plasma Bodies⇒Tag antigen
  • extracellular pathogens
22
Q

What is cell-mediated immunity?

A

Cytotoxic T cells and NK cells destroy virus-infected cells

  • Assisted by non-lymphoid effector cells (macrophages, neutrophils, eosinophils) that directly eliminate a variety of microbes (e.g. phagocytosis)
  • intracellular pathogens
23
Q

What is the difference between a BCR and an Antibody?

A

BCRs are expressed by B cells

  • surface Ig
  • have transmembrane region

Antibodies are secreted by plasma cells

  • soluble Ig
  • no transmembrane region

The Fc region is where the different Ig Isotypes occur

24
Q

What are the different antibody mechanisms?

A
  1. Virus and Toxin Neutralization
  2. Opsonization
  3. Complement forms Membrane Attack Complex
  4. Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC)
25
Q

How do innate immune cells and antibodies interact?

A

The Fc region of the antibody doesn’t bind the antigen and interacts with receptors on the innate immune cell called FcR

-the FcR recognizes the specific Ig Isotype expressed in the Fc region of the antibody

26
Q

What is the antibody mechanism virus and toxin neutralization?

A

The antibody binds the pathogen and prevents pathogen from binding to host

27
Q

What is the antibody mechanism opsonization?

A

All phagocytes have FcR’s mostly for IgG

  • the IgG opsonizes the pathogen tagging
  • when the phagocyte binds the Fc with its FcR it will phagocytose the tagged pathogen
28
Q

What is the antibody mechanism complement fixation and formation of the membrane attack complex?

A

C1q recognizes the Fc of the antibody that is stuck to the pathogen

  • Membrane Attack Complex is formed on pathogen
  • lysis or phagocytosis
29
Q

What are the different regions of the antibody responsible for?

A

Fab

Antigen-binding site

Affinity selection

Fc

Molecular interactions (complement, FcR)

Class switching

Isotypes (IgA, D, E, G, or M)

30
Q

Which Ig Isotypes are pentameric and dimeric?

A

Pentameric = IgM

Dimeric = IgA

31
Q

Which FcRs bind the IgG isotype and what is their function?

A

FcR = FcγRI, FcγRIII, FcRn

FcγRI - phagocytosis by macrophages, DCs, and neutrophils; activation of granulocytes

FcγRIII - ADCC by NK cells

FcRn - Transcytosis of antibodies across placenta and from milk to blood in infact intestines

32
Q

Which FcRs bind the IgE isotype and what is their function?

A

FcR

-FcεRI

FcεRI

-Degranulation of mast cells, basophils, and eosinophils

33
Q

Which FcRs bind the IgA and/or IgM isotype and what is their function?

A

FcαRI binds IgA

pIgR binds IgA and IgM

FcαRI - phagocytosis, ADCC, activation of granulocytes

pIgR - trancytosis of antibodies from blood to mucosa

34
Q

What does pentameric IgM do?

A

Complement Activation

  • attaches to surface of microbe
  • C1q recognizes and forms MAC in classical pathway
35
Q

What does monomeric IgG do?

A

Most abundant in blood due to memory

-maternal IgG crosses placenta

Can do following:

  1. Neutralization
  2. ADCC
  3. Opsonization and Phagocytosis
  4. Classical Complement Pathway
36
Q

What does dimeric secretory IgA do?

A

Mucosal Immunity

  • TH2 activation of B cells
  • Neutralization
  • transferred into breast milk for passive immunity
37
Q

What does monomeric IgE do?

A

IgE primes inflammatory cells

  • Fcε​RI are on mast cells and eosinophils
  • TH2 activation of B cells
  • IgE binds antigen and cause inflammatory cells to release histamine
  • anti-parasite response
38
Q

How are cytotoxic T lymphocytes and Natural killer cells similar?

A

Both produce:

Perforin - punch hole in membrane of infected cell

Granzymes - go thorugh hole and chew up virus and host cell machinery disrupting the cell and inducing apoptosis

BIO 320 Immunology (13 decks)

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