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Immunology > B- Cell Mediated Immunity > Flashcards

B- Cell Mediated Immunity Flashcards

1
Q

*Understand crosslinking of B-cell receptor and downstream signaling
Igα, Igβ, Blk, Fyn, Lyn, Syk

A

1.Naive B cells- have surface Ig M molecule that cross-links BCR (clustering)
2. This leads to activation of Tyrosine kinases (phosphorylate ITAMs,)
Ig Alpha and Ig Beta- are associated with IgM; the cytoplasmic tails are phosphorylated (contain ITAMs) by Blk, Fyn, Lyn- tyrosine kinase
3. Syk then binds to Ig Beta tail- signaling cascade and changes in gene expression

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2
Q

*Know the components of B-cell co-receptor and their function

A

Since cross-linking of B-cell receptor is NOT sufficient to activate Naïve B-cells. You need B-cell co-receptor.
B-cell co receptor: CD21 or CR2 (recognizes iC3b and C3d on pathogens with CR1)
CD19- signaling portion
CD81 - brings CD19 to surface; organizes B-cell and co-receptor interaction.
CR1- binds C3b on the pathogen, cleavage by factor I to iC3b and C3d

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3
Q

*Know the role of follicular dendritic cells

A

Follicular dendritic cells (FDCs)= secondary lymphoid organs- stromal cells of fibroblast- like origin, NOT hematopoietic origin
FDCs organize the B-cell area of the lymph node into PRIMARY FOLLICLES - interdigitating dendrites
FDC have extensive surface area- large quantities of antigens can accumulate
Long ‘stalk” shape allows CR2 to “fish” or search for antigen.

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4
Q

*Know the role of CCL21, CCL19, CXCL13, CCR7, CD40 ligand, CD40 receptor,
LFA-1, ICAM-1, AID, in B-cell activation

A 
CCL21, CCl19
CXCL13
CCR7
CD40 ligand and CD40 receptor
LFA-1 
ICAM-1
AID in B-cell activation
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5
Q

*Know the role of Sphingosine 1—phosphate and CD69 in B—cell exit from the
lymph node

A

Sphingosine 1-phosphate
CD69
B-cell exit from lymph node

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6
Q

*Understand how B-cell migrate between primary follicle, T-cell area, and
medullary cords and what occurs in each area

A

primary follicle
T-cell area
medullary cords.

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7
Q

*Know the difference between centroblasts and centrocytes – division and
immunoglobulin expression

A

Centroblasts- RAPIDLY DIVIDING B cells, that create DARK zone of germinal center
centroblasts give rise to centrocytes (they become small centrocytes after stopping division and maturing)
Centrocytes- Slowly dividing B cells that form light zone of germinal center. They express cell surface immunoglobulin (Ig E?) which has acquired mutations and isotype switching, now in light zone (interact with FDCs that have antigens)

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8
Q

*Know consequence of IL-10 versus IL-4 expression during B-cell activation

A

During infection- IL-10 production by TFH cells induces centrocytes to differentiate into PLASMA cells (which make antibodies that fight and terminate current infection)
As infection CLEARS- IL-4 produced by TFH cells, and induces centrocytes to become MEMORY cells (prevent future infection from causing disease)

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9
Q

*Know the general functions of the various immunoglobulins – area(s) of the
body they protect/pathogens they protect against, affinity, and downstream
events – focus on what we discussed in class

A

A

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10
Q

Which cytokine augments the production of Ig A?

A

cytokine IL-5 augments production of IgA

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11
Q

Describe where Dimeric IG A comes from and its role

A

Dimeric Ig A- Protects the Mucosal epithelial surfaces
Made in patches of mucosal-associated lymphoid tissues (MALT)
antibody secreting mucosal cells are on one side of mucosal epithelium and pathogen is on the other.

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12
Q

Which immunoglobulins collectively prevent blood-borne infections and spread of microorganisms?

A

IgG and Monomeric IgA

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13
Q

How is Ig G and monomeric Ig A formed? What is the dominant blood borne antibody (Ig molecule) ?

A

Ig G and MONOMERIC IgA are produced by ISOTYPE SWITCHING and AFFINITY MATURATION
-two-high affinity binding sites
-better able to infiltrate tissue than IgM
Ig G- DOMINANT blood-borne antibody
Monomeric IGA- made by B cells in lymph node and spleen
these two IG’s collectively prevent blood-borne infections and spread of microorganisms.

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14
Q

What are neutralizing antibodies? What happens to person with Ig A antibodies vs someone without virus antibodies?

A

Neutralizing antibodies- HIGH-AFFINITY antibodies that PREVENT microbial attachment to target cells- coat pathogen and prevent infection of target cells
adult with virus antibodies - Virus cannot infect cells, person is healthy
another person Without antibodies- Virus infects cells and replicates; person gets severely sick for 2 weeks).

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15
Q

What role does TFH cells play in B cell maturation? What are the two stages of B-cell activation?

A

TFH cells remain in secondary lymph tissue and activate naive B cells to develop into mature antibody producing plasma cells.
2 stages of B cell activation:
1st priority- Speed of production- Ig M antibody- low-affinity
2nd priority-
1. increase the affinity of antibody through somatic hypermutation
2. Change the isotype of the antibody- recruit effector cells and mechanisms that can clear the infection.

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16
Q

What changes occur when B-cell receptor and co-receptor engage?

A

once BCR and co-receptor engage the pathogen, Lyn phosphorylates CD19 (Lyn bound to Ig alpha); resulting in activation of synergistic signals and changes in gene expression in nucleus.

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17
Q

Explain the main cells that take up antigens expressed on FDCs and subscapular sinus What are C3d and C3b?

A

both CR2 and MACROPHAGES take up antigens from the lymph
CR1- attaches to C3b
CR2- attaches to C3d
C3d- and C3b- are Tagged antigens that are presented at the surface
Long “stalk” allows CR2 to “fish” (look/capture) for antigen
Macrophage- bind soluble antigens.

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18
Q

Differentiate between what occurs when T cell vs B cell encounters an antigen?

A

Naive B cells:
1. search for specific antigen displayed by FDC in B-cell area
2. Antigen activated B cell will move To BOUNDARY region
3. Antigen-activated B cell present antigen to Effector TH cells, forming cognate interactions and cognate pairs
Naive T cells:
1. Search for specific antigen presented by DENDRITIC cells in the T cell area
2. Antigen-activated T cell proliferates an differentiates.

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19
Q

Explain how naive B cells are able to enter lymph node. Also describe what occurs if antigen is encountered vs Not encountered. When will cell enter follicle?

A

Naive B cells attracted to lymph node by CCL21 and CCL19 and into the B-cell follicle by CXCL13
Then they enter the subscapular sinus- subscapular sinus macrophages will present antigen; will enter follicle if antigen is encountered and interacts with TFH.
If NOT antigen encountered: naive B-cells enter follicle and “search FDCs” for antigen
If antigen encountered: B cell expresses CD69 (NO S1P receptor expression)

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20
Q

What happens once you have antigen-activated B cell. What are the roles of CCR7 and CCL21, CCL19? What decreases the expression of CCR7? What is CD40 used for?

A

Antigen-activated B- cells begin to endocytose and process the BCR-antigen complex, then present peptides on MHCII.
CCR7 expression is induced- which binds to CCL21 and CCL19. B cells move to boundary between B and T cell areas- interact with TFH cells.
TFH cells DECREASE the expression of CCR7- they move to the boundary.
If conjugate pair is formed, T cells are induced to express CD40 ligand which binds to CD40 on B-cell and leads to transcription of NFkB and ICAM-1 (synapse formed)

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21
Q

What occurs during the cognate interactions with naive B cells?

A

process

  1. Helper TFH cell conjugates with B cell and begins to synthesize cytokines and CD40 ligand
  2. The helper TFH cell reorients the cytoskeleton and secretory apparatus toward the B cell
  3. Cytokines are secreted into the narrow space between the TFH cell and the B cell (synapsis)
  4. TFH cells recognize an antigen presented by B cell and initiates conjugate formation
  5. talin concentrates at urea of cell-contact
  6. Cytokines made by the TFH cell are secreted onto the B cell surface
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22
Q

compare and contrast where expansion occurs for antigen activated B cells. What is a germinal center?

A

Primary focus for expansion of antigen-activated t cells: occurs in MEDULLARY cords
Secondary focus for expansion- occurs in PRIMARY FOLLICLE
Expansion of antigen-activated B cells in the primary follicle leads to formation of GERMINAL center

23
Q

Describe how B-cell and TFH conjugate pairs move to meduallary cords, and what occurs during this time. How long does this process last? What is the result?

A

B-cell/TFH conjugate pairs move into medullary cords and begin to divide- PRIMARY FOCUS
- This lasts several days and gives rise to dividing to B cells secreting Ig-M (antibody leaves via efferent lymph and is delivered to blood to be carried to site of infection)

24
Q

What could occur to B cells that stay in medullary cords? What is a BLIMP1?

A

B cells that stay in the medullary crowd differentiate into PLASMA CELLS due to Il-5 and IL-6 secreted by TFH cells.
BLIMP1- transcription factor that induces B-cells to STOP DIVIDING and INCREASE Immunoglobulin chain synthesis and secretion

25
Q

What is the role of plasma cell? What percent of protein is Immunoglobulin?

A

plasma protein- antibody factory

20% of protein production is Immunoglobulin- rough ER.

26
Q

Explain whether or all B-cells become plasma cells and their roles.

A

NOT all B cells become plasma cells.

some move to primary follicles of B-cell area with TFH attached.

27
Q

Describe what occurs in the germinal center reaction?

A

Germinal center reaction:

  • DFC (dendritic follicular cells) produce IL-6, IL-15, 8D6 and BAFF- cytokines that induce B-cells to divide rapidly and become centroblasts, creating the germinal center.
  • TFH cells also divide- interaction at CD40 causes B-cells to produce AID (essential for hypermutation and isotype switching)
  • primary follicle is now a secondary follicle- causing swelling of lymph nodes (after infection)
28
Q

Elaborate on the different zones of the germinal center, including the mantle, dark ,light zones and centroblasts.

A

Mantle Zone- area where NAIVE B cells pass through LYMPH node
Dark Zone- compact area of densely packed CENTROBLASTS
Centroblasts give rise to centrocytes- divide more slowly and begin to express surface immunoglobulins again(mutated and isotype switched)
Centrocytes- SHORT-LIVED unless they encounter antigen and bind TFH.
Light Zone- LOW Density of centrocytes and HIGH density of FDCs and TFH cells.

29
Q

Explain what occurs when an activated B cell undergoes somatic hypermutation. What occurs as a result? What is the role of centrocytes?

A

When activated B cell cell undergoes Somatic hypermutation: creates DIVERSITY; high and low affinities
Centrocytes with the Highest affinity for antigen on FDCs should OUT COMPETE the others.
Centrocytes will process antigen via MHCII and then create synapse with TFH- inducing survival signals in centrocyte and differentiate into plasma cells.

30
Q

Differentiate between the plasma cells that are in the lymph node vs bone marrow?

A

Plasma cells remain in LYMPH: SHORT-lived
Plasma cells remain in BONE MARROW: LONGER lived
Affinity maturation- refines the response to this pathogen.

31
Q

Describe the two main outcomes that can occur during somatic hypermutation for B cells.

A

In activated B cell:
Somatic hypermutation of IG V regions will occur in proliferating germinal center centroblasts.
outcomes
1. Centrocyte dies by Apoptosis- if germinal center centrocyte binds with LOW affinity surface Immunoglobulin. B cell receptor is NOT cross-linked and centrocyte does not present antigen to TH cell.
2. Cell differentiates into plasma cell: if germinal center centrocyte with High-affinity surface IG
B cell receptor is cross-linked and antigen is presented to helper TFH cell. Centrocyte survives, divides- plasma

32
Q

What occurs in a lymph node with hyperIG M syndrome (No germinal centers)?

A

A patient with Hyper Ig M syndrome: deficient in CD40 ligand.
no germinal centers
-NO isotype switching- due to lack of CD40 ligand, B cells cannot switch Ig isotype, leading to individual having abnormal amounts of IgM
-poor antibody responses to antigen.

33
Q

Which cytokine augments the production of IgA?

A

IFN-y augments the production of IgA

34
Q

Describe what occurs in centrocytes with identical B-cell receptors. What are the different outcomes that occur?

A

TFH cell that secretes IL-10, allow centrocytes to differentiate into plasma cells
plasma cells- make antibodies that fight and terminate current infection
TFH cell that secretes IL-4, allow centrocytes to differentiate into MEMORY B cells and prevent future infections from causing disease (investment)

35
Q

Differentiate between the intrinsic and inducible properties of Naive B cell and Plasma cell.

A

Naive B cell- has both intrinsic (surface Ig, Surface MHC Class II) properties and Inducible (growth, somatic hypermutation and isotype switch).
Plasma cells- have only one Intrinsic property (HIGH-RATE Ig SECRETION). Plasma do not respond to antigen, hence do not have any other properties.

36
Q

Describe the characteristics of IgM, and its functions.

A

IgM- FIRST ANTIBODY produced by plasma cells
10 antigen binding sites
-binds Microorganisms and particulate antigens and activates COMPLEMENT cascade
-BULKY and has limitations in passively leaving the blood.

37
Q

elaborate on IgM’s involvement in the complement cascade

A

Ig M involved in INITITATION of Classical pathway of COMPLEMENT by IGM binding to antigen on pathogen surface.
Then cascade occurs with C2 and C4 being cleaved and forming complex, C3 convertase being made.

38
Q

What is the role of IgG and Monomeric IgA?

A

IgG and MONOMERIC IgA: produced by ISOTYPE Switching and AFFINITY Maturation
-two high-affinity binding sites
-Better able to infiltrate tissue than IgM
IgG- DOMINANT Blood-BORNE ANTIBODY
Monomeric IgA: made by B cells: in LYMPH node and SPLEEN.
collectively, the IgG and monomeric IgA prevent blood-borne infections and spread of microorganisms.

39
Q

Describe the process of Fluid-phase endocytosis of Ig G.

A
  1. Fluid phase endocytosis of Ig G from the blood by endothelial cells of blood vessel
    2, Acidic pH of endocytic vesicle causes the association of IgG with FckrRn, protecting it from proteolysis.
  2. upon reaching basolateral face of endothelial cell, basic pH of extracellular fluid dissociates IgG from FckRn.
40
Q

What is major role and function of Dimeric IgA?

A

Dimeric IgA- protects the MUCOSAL epithelial surfaces
Made in patches of mucosal-associated lymphoid tissue (MALT)
ANTIBODY-SECRETING MUCOSAL cells are one side of mucosal epithelium and PATHOGEN is on the other.

41
Q

Describe the transcytosis process of dimeric IgA in epithelial cell.

A

Dimeric IgA:

  1. Dimeric IgA binds to PlgR receptor on basolateral face of epithelial cell
  2. receptor-mediated endocytosis of igA (forming vesicle)
  3. Transport of IgA to apical face of epithelial cell
  4. Receptor is cleaved, IgA is bound to mucus through the secretory piece.
42
Q

What is the role of neutralizing antibodies? provide an example.

A

Neutralizing antibodies: High-affinity antibodies that prevent microbial attachment to Target cells- coat pathogen and prevent infection of target cell
example:
adult with anti-influenza virus Ig A antibodies- Virus will not be able to infect cells, student remains healthy
Twin sister without anti-influenza virus antibodies: Virus infects cells and replicates. Twin sister gets severely sick for two weeks.
neutralizing antibodies- block binding of toxin to cell-surface receptor

43
Q

Explain how antibodies may help with bacterial infections in children.

A

Control bacterial infection:
control Streptococcus pyogenes population in pharynx
Children with antibodies against s. pyogenes: antibodies prevent attachment of bacteria to tissue: bacteria swept to the gut. Bacteria population is limited and kept at a steady state: healthy
children WITHOUT antibodies against S.pyogenes:
- Bacteria stays in the pharynx and multiplies
-Bacterial population expands out of control and damages its environment: suffer sore throat.

44
Q

Which Immunoglobulins are capable of neutralizing toxins? How do they do this. What is required for antibodies to neutralize?

A

IgG (tissue) and IgA (mucosal Surface) can NEUTRALIZE some microbial toxins and animal venoms.
To neutralize, Antibodies must be HIGH-AFFINITY, bind IRREVERSIBLY, and PENETRATE tissue to reach toxin.

45
Q

What is another immunoglobulin (besides IgM) that can activate complement pathway? How many pathways are available?

A

IgG - can activate Complement pathway
process:
1. IgG molecules bind to antigen on bacterial surface
2. C1q binds to two or more IgG molecules and initiates complement activation
Another path:
1. Ig G molecules binds to soluble MULTIVALENT antigen.
2. C1q binds to soluble immune complex and initiates complement activation.

46
Q

Describe the role of erythrocytes in immune system.

A

Erythrocytes facilitate the REMOVAL of IMMUNE complexes from the blood
process:
1. small antigen: antibody complex forms in the circulation and activates complement
2. Immune complex is coated with covalently bound C3b
3. CR1 on erythrocyte surface binds C3b-tagged immune complex
4. Erythrocyte carries immune complex (C3b, antigen:antibody) to liver or spleen, where complex is DETACHED and taken up by MACROPHAGE

47
Q

What is the role of phagocytes in immune system?

A

phagocytes UPTAKE and BREAKDOWN Antibody-coated pathogens
process:
1. antibody binds to bacterium
2. Antibody-coated bacterium binds to Fc receptors on cell surface
3. Macrophage membrane surrounds bacterium
4. macrophage membranes fuse, creating a membrane-enclosed vesicle, the PHAGOSOME
5. Lysosomes fuse with phagosome , creating PHAGOLYSOSOME and degrading pathogen.

48
Q

Explain how Natural Killer (NK) cells are able to kill target cells.

A

NK cells recognize IgG-COATED target cells
process:
1. Anti-CD20 antibody binds to CD20 (antigen) on surface of B-cell lymphoma cell
2. Fc receptor on NK cell recognize bound anti-CD20 antibody.
3. Cross-linked Fc receptors signal NK cells to KILL the B-cell lymphoma cell
4. B-cell lymphoma cell dies by apoptosis.
Fc receptor (Fc-gammaRIII, CD16)

49
Q

What is the role of IgE and its functions? What is the use of mast cells?

A

IgE- used as cell-surface receptor for antigens- where CROSS-LINKING on MAST cells results in granule release of inflammatory mediators (histamine)
-Mast cells secrete mediators that cause sneezing, vomiting, coughing, diarrhea- to EXPEL pathogen from respiratory and GI tract.

50
Q

Differentiate between an inactivated mast cell and an antigen-activated mast cell.

A

Inactivated mast cell- has preformed granules containing histamine and other inflammatory mediators, (also antibody Ig E bound to Fc receptor)
Antigen-activated mast cell- has MULTIVALENT antigens CROSS-LINKS IgE antibody bound at mast cell surface (IgE bound to Fc receptor) RELEASING Granule contents

51
Q

Explain how eosinophils can attack a schistosome parasite.

A

Eosinophils can attach to parasite through specific binding of Fc receptor( FcEpilson Ri ) and IgE antibody.
Process:
1. IgE antibody will bind to antigen on Schistosome
2. Eosinophils will attach to Fc receptor that is attached to IgE.
3. causes granulation of eosinophil, pouring the toxic contents of granule onto parasite surface.
Schisotosome- parasite of trematode worm

52
Q

What are the general functions of the different immunoglobulins? What areas of the body do they protect? which pathogens do they protect against?

A

Dimeric IgA- predominates in secretions at mucosal epithleila
Monomeric IgA- made by B cells activated in the lymph node or spleen; smaller size allows it to penetrate tissues better than other Igs. Has high affinity binding site
IgM- secreted as pentamer in plasma cells
activates complement pathway, 10 antigen-binding sites
IgE- made in small amounts, mostly found in connective tissue of mast cells, mucosal surfaces. It aids in ejection of pathogens and toxic substances
IgG- dominant blood-borne antibody; high affinity binding site, and is able to penetrate tissues better than other Igs. IgG is transferred from mother to fetus across placenta

53
Q

Explain how some immunoglobulins are transferred to infants before, and after birth.

A

During prenatal development in mother’s womb: fetus cannot make its own Immunoglobulin .
Hence, IgG from mother CROSSES placenta to transfer IgG to fetus for protection against infection.
IgG (protective antibody) transported to fetus
After birth: When mother is breastfeeding, the infant will obtain Dimeric IgA from mother’s milk.
IgA will then be transferred to infant’s GUT (where IgA binds and prevents microorganism from attaching to gut epithelium) for PROTECTION
PASSIVE transfer: infant obtaining Dimeric IgA from mothers breast milk and IgA transferred to infant gut.

54
Q

Describe the timeline of the change in Ig levels for infants. What time frames is IgG Lowest?

A

maternally derived IgG relatively low from conception all the way to birth of child and will further increase once it has been 6 months since infant’s birth. Then it will decrease when infant is 1 years old.
Ig G levels are LOWEST in infants aged 3-12 months.
After 6 months: infant will develop immune system that produces its own antibody
newly synthesized Ig A and Ig G and Ig M will increase after 1 years old.

Immunology (11 decks)

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