L6- The humoural response

what is another name for antibody

Immunoglobulin (Ig)

Parts of antibody

what is epitope

Epitope is on pathogen anitigen binds to partope on antibody

Differnce between BCR and antibody

Antibody is the secreated form of B cell reseptor - they are basically the same thing

How do we get B cells actiavtion

T cell dependant response (More common)

• Antigen binds to BCR → 1st activation signal

• peptide presented on MHC, T cell binds, if strong binding through help of assesory protiens liek CD40, CD40L get 2nd activation signal stops B cell form undergoing apoptosis

and T cell independant response

• same 1st signal

• but 2nd signal is from activatin TLR on B cell

Transmembrane → secreated

DNA starts off with; VDK regions, constant regions and trasmembarane regions

• B cell starts off by removing nay unused VDJ regions noy being used

• as moves ot plasma blast removes trasmembrane regions

• this is why cannot go back to being B cell affer now a plasma blast no longer express BCR

class switch

happens in Niave B cells

• before all express IgM or IgY both look same on surface membarne

when class switch happens

• cut out constant regions IgM and IgY with enzyme AID

• to add IgG, IgA, IgE

• non reversible

• happens due to environmnet

IgM

• first responder

• usually as a pentomer as then has higher avidity (alone has low affinity)

• good at triggering phagocytosis and activating complement

• made in blood, milk, mucous, saliver

IgA

• local task force

• higher affinity as post germinal center

• exists ad dimer, tetrimer or heximer

• in secreations, lung, mucosa

• improtant in gut - neytralises pathogenic bacteria in gut

IgG

• Specelised task force

• High affinity as post germinal center

• exists as diner

• mostly foudn in blood

• good at neutralisation and activating complement

• different type IgG1,2,3,4

• improtant in vaccination

• only Ab that can cross the placenta

what happens in germinal center

• its in lymph nodes

• have Dz and LZ

• GZ ahve proliferation and amplification and muatations of BCR

• then they move to LZ where they encounter antigen - if have good binding with antigen and tehn TCR then no apoptosis if bad binding then get apoptosis

• thoes BCR that survive go back to DZ to proloferate t

• they under go mutations on DNA level by AID enzyme, cuts things out helping them get better at binding antigen

• this is somatic hypermuatation

• if muattaion makes it worse than die by apoptosis

• then surviving B cells will exity to be antibody producing cells and produceing high affinty IgG

IgE

• low amounts in serum

• exists as dimer

• binds to Fc receptor leading to degranulation of histoamines leading to coughing, sneezing..

• effective againts paracites

IgD

• not much knonw

• maybe like IgE binding to Fc recptor

• low amounts is secreated in blood

  • mainly used a s a marker to identify niave B cells

What are the things antibody can do when binds to target

• neutralisation IgG

• Optimization IgG

• Antibody Dependant Cellular Cytotoxicity IgA/IgG

• complement IgM

Neutralisation

• antibody binds to part of virus that is needed to enter the cell

• so it blocks entry

• e.g. In HIV antobodies can bind to part of virus that bonds to human CD4 cells

Fc receptors

phagocytes binds to FC receptors which allow phagocytosis to happen

• happens by binding to Fc gamme (IgG)

Antibody Dependant Cellular Cytotoxicity

Complement

antibody binds to pathogen activating C1Q in classical pathway