adaptive immunity - b cell Flashcards

1
Q

b cells are part of the — immune system as they have —- response
they produce – which is crucial to fight pathogens ( mainly extracellular pathogens)

A
  • adaptive
  • antigen specific
  • antibodies
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2
Q

-BCR are found in the cell —- receptor or b cells and they recognise antigen in —- form
-anitgen recognition cause b cell – where they — and differentiates into —
each plasma cell product trillions of —-
- the — are the secreted form of the BCR (which is a membrane bound immunoglobulin molecule )
- antibodies are secreted into — and – which triggers effector response

A
  • cell surface antigen receptor
  • biological form ( protein carbs lipids polysaccharides )
  • b cell activation
  • proliferates
  • differentiates into plasma cells
  • antibodies ( aka immunoglobin aka ig)
  • antibodies
  • circulation
  • mucosal membranes
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3
Q

life cycle of b cells :
1- b cell development occurs in — and its – to antigen exposure:
* BCR rearrangement
* Selection process
* Now known as Naïve B cells
2- b cell activation occurs in — and its — antigen exposure :
* B cell is ACTIVATED
* Differentiation into
plasma cells
3- b cell function occurs in— and its – to recognition antigen

A
  • bone marrow aka primary lymphoid antigen
  • prior
  • lymph nodes . spleen aka 2ndart lymphoid tissues
  • initial
  • peripheral tissues where needed
  • response to
    ( check slide 9 )
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4
Q
  • A membrane bound IgM is also called the —
  • It is composed of— chains and —- chains
    and —- chains
  • They are assembled to form a — structure
  • The heavy and light chains are attached via—- bonds
  • The — region is the variable ‘antigen-binding site’
  • The — region is the constant region
A
  • BCR
  • 4 polypeptides
  • 2 heavy chains (H) and 2 light chains ( L)
  • Y
  • disulfied bonds
  • v region
  • c regions
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5
Q
  • At any one time we have millions of B cells in our body, each having a
    BCR with a different—- for antigen
  • How? During B cell development—- of BCR genes (VDJ
    recombination) occurs and variable BCRs with unique specificities are
    generated!
  • —–– randomly combine V(D)J genes to form VDJ or VJ
    segments →—- different combinations!!!!!
A
  • specifity
  • gener rearrangement
  • CDJ recombination
  • 10 power 11
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6
Q

b cell activation occurs in 2 ways:
1- — > which use antibody class isotope-switched high affinity antibodies , memory b cells , long lived plasma cells
2- —> mainly IgM ,low affinity antibodies , short lived plasma cells

A
  • T cell dependent ( as follicular b cells )
  • T cell independent ( as b-1 cells , marginal zone b cell )
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7
Q

b cell activation requires — signals
1- singnal : — binding to BCR
*B cell antigen receptor will recognise—- (protein, carbohydrate, lipid, polysaccharide)
*Triggers—- of antigen
*B cells excellent—- and—-
*If T-independent, the recognition of an antigen is — to activate the B cells to produce— levels of IgM antibodies (no second signal)
*If T-dependent (i.e. protein antigen), peptides are presented on MHC class —
*Up-regulation of CD40 a co-stimulatory receptor
*Up-regulation of cytokine receptors
2d signal:
use — help
* ACTIVATED —- will recognise antigen presented by B cells
* The T cell upregulates costimulatory molecules —- which binds to —on —
* The production of— drive B cell proliferation and differentiation

A
  • 2 signals
  • antiges
  • antigens
  • phagocytosis
  • phagocytes and APC
  • enough
  • low
  • class ii
  • T cell help
  • helper T cells
  • CD40L
  • CD40
  • b cells
  • cytokines
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8
Q
  • —- are secreted proteins which recognise — on the surface of pathogens using their antigen binding site within the variable regions
    *—- can be any biological molecule –protein, carbohydrate, lipid, polysaccharide
  • The—- region activates different effectors (complement proteins or innate immune cells) that eliminates these microbes and toxins
  • The ‘type’ of— region defines the isotype of an antibody
A
  • antibodies
  • epitopes
  • epitopes
  • constant
  • constant
    ( info : The “epitope” is the specific part of the antigen that is
    recognised by T and B cell receptors)
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9
Q

b cell function occurs in — where needed and the functions include :

A
  • peripheral tissue
    1- neutralisation of microbes n toxins by igG igA
    2- opsonisation and phagocytosis of microbes IgG
    3- antibodies dependent cellular cytotoxicity IgG (igE)
    4- phagocytosis of mcuorbes opsonisation w complement fragment ( c3b) , activation of complement (IgG , igM)
    5- inflammation
    6- lysis of microbes
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10
Q

antibodies structural features:
1. —–: recognises antigen and binds incredibly tightly – Incredibly specific – can distinguish between very similar epitopes
2. ——:where — protein binds to start the classical complement cascade
3.binding site for —- Macrophages, mast cells,basophils, NK cells, neutrophils and eosinophils all have Fc receptors that will recognise the
Fc portion of an antibody and
bind helps antibody function

A
  • anitgen binding site
  • complement biding site
  • C1q
  • immune cells
    ( check slide 23 structure sssosooso important )
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11
Q

b cell activation results in :

A
  • antibodies secretion
  • isotope switching where only when T cell dependent
  • affinity maturation when only T cell dependent
  • memory b cell only when T cell dependent
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12
Q

—- anything the immune system recognises as non self

A

antigen

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12
Q
  • — is the first antibody secreted upon infection
  • But B cells can isotype switch into making ——- isoforms as required
  • During isotype switching the antigen binding site remains —- but the constant region of the heavy chain is —-
  • The process of isotype switching is induced by —– interaction and—- released by T helper cells
  • Each isotype has a slightly different function as discussed later
A
  • IgM
  • igG igA igE igD
  • same
  • replaced
    -CD40-CD40L
  • cytokines
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13
Q

—- complement activation
—- oponiszation , phagocytpsis , complement activation , neonatal immunity ( placental transfer )
—– immunity against helminths , mast cells degranulation ( immediate hypersensivity )
—- mucosal immunity ) transpot IgA through epithelia )

A

IgM
IgG ( most skilled ) IGG1 IGG3
IgE , IgG4
- IgA

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14
Q
  • —- is the process by which the
    affinity of antibodies produced in response to an antigen increases with— or—- exposure
  • With repeated exposures to the same antigen, a host will produce antibodies of successively—- affinities
  • A secondary response can produce antibodies with several fold — affinity than in a primary response
  • one way this occurs is by —- in the variable antigen binding region of the antibody
A
  • affinity maturation
  • prolonged
  • repeated
  • great
  • great
  • random mutation
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15
Q

pathogens neutralisation :
* Antibody neutralization of microbe and toxins
* Binds microbes/toxins and makes them —to enter cells
* Neutralization function of antibody
requires only the —- regions of antibodies, not the — region
* Very efficient at preventing —

A
  • too bulky
  • antigen binding region
  • not Fc region
  • viral infection
16
Q
  • Antibodies can “coat” microbes and make it easier for— to recognise them
  • The opsonised microbe will bind to —- on the phagocytes
  • This leads to efficient phagocytosis and killing of the internalised microbe
A
  • phagocyte
  • antibody specific receptors
    ( Neutrophils, Macrophages and dendritic cells all have Fc receptors for IgG and phagocytose IgG coated pathogens)
17
Q

complement activation:
Antigen binding site and complement
recognition sites needed
* Antibody binds to pathogen surface (typically IgG/IgM)
* Complement binding site exposed
* Get activation of the complement cascade (classical pathway), generating products thatcan:
- Attract leukocytes → —-
- Opsonise microbes →—-
- Cause assembly of the MAC → —

A
  • inflammation
  • promotes phagocytosis
  • lyse bacteria
18
Q

antibody dependent cellular cytotoxity:
* —- cells and other —bind to antibody-coated cells and destroy these cells
* NK cells express FcγRIII receptor which binds to IgG attached to the surface of a cell
* NK cells discharges — to kill opsonised cell
* Some therapeutic antibodies use this mechanism to kill —-

A
  • nk cells and other leukocyte
  • granules
  • cancer cells
19
Q
  • Most— are too large to be
    phagocytosed
    *— antibodies are generated against the worms
  • IgEs bind to (“prime”) the surface of either —- or —- (via Fcε receptors)
  • When the worm antigens bind to their
    specific IgE antibodies, this perturbs the
    membrane of the mast cells/eosinophils
  • These cells —- , releasing their
    contents, which can kill the worms
  • Mast cells , histamine and proinflammatory mediators; eosinophils – lytic granules and
    proinflammatory mediators
A
  • helminth
  • IgE
  • mast cells or estinophils
  • degranulates
20
Q

antibody classes:
they have – types of heavy chains
* most abundant Ig in the body; only antibody class that can cross
placenta; involved in all antibody functions aka —-
* Secreted at mucosal surfaces; blocks pathogen entry; involved in
neutralisation; IgA immunity acquired via colostrum and milk aka —-
* On naïve B cells; first Ig to be secreted; involved in complement activation aka —
* Part of antigen receptor on naïve B cell surface; unclear role (binds mast
cells and basophils and drive the production of anti-microbial peptides) aka —
* Attaches to mast cells and eosinophils; implicated in worm expulsion and
classic allergic responses aka —-

A
  • 5 ( gamma alpha mu delta epsilon )
    IgG
    IgA
    IgM
    IgD
    IgE
    ( check slide 36)
21
Q

read:

A

B cell/Antibody Deficiencies
Common Variable Immune Deficiency (CVID)
* Characterised by low antibody levels, specificially IgG, IgM and
IgA
* Symptoms vary but recurrent infections of the lungs and
gastrointestinal tract are more common
Selective IgA Deficiency
* Most common immunodeficiency
* Failure of B cells to differentiate into IgA producing plasma cells
* At least 1/3 patients are asymptomatic (as IgM can compensate)
X-linked agammaglobulinemia (XLA)
* Caused by a mutation in a protein involved in B cell
development → Absent B cells
* Recurrent bacterial infections