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Ocular blood collection  bleed the eye

Internationally approved

Go through animal handling course  caught not: jail up to 1 year + fine


Bigger the number, smaller the syringe



Van der waal


1011 type of B cells  capable of dealing with 100 trillion types of antigens

 Different 1011 FAB regions

Primary antibody response: Clonal expansion and differentiation of cells

Secondary response: memory B cells recognize  response much more rapid 

more antibodies (of higher affinity) are produced by plasma cells

Antibodies will be degraded  made of proteins  all proteins can be degraded

in the body
Once it’s bound to antigen, it will be used up.

Denaturation  no longer useful for detecting or neutralizing any pathogens

More effective to receive vaccination 2 weeks prior to exposure to pathogens in


 Body takes time to develop B memory cells

 A month! (to be safe)

Amount of antibodies reflects amount of antigens being injected.

Amount of proliferation depends on amount of antigens

Why need few days for B cells to produce antibodies (time lag)?

What receptors are found on B cells that will help recognize the antigens?

- Antibodies present on B cells (IgM then IgD)

- IgM is the default antibody that will accept the antigen

- Then followed by IgD

Presentation of antigen fragments to T helper cells

Structure that presents to T helper cells major histocompatibility complex (MHC)

Cytokines produced by T helper cells

Cytokines to activate the B cells to divide (into larger number) and differentiate
into B plasma cells and B memory cells

CD4+  a kind of receptor protein on B cells  recognize CD4 ligands (CD4L) on

the T helper cells

Plays a part in presentation of antigen to T helper cells

Epitope  on antigen

Paratope  on antibodies

Introduction of new antigens  lead to clonal selection  a large pool of memory

cells, antibodies, plasma cells that will produce antibodies to deal with the
immediate reaction of the antigens

Those B cells that recognize cell antigens will be eliminated

 Use their own antibodies to attack cells

So supposedly, more than 1011 B cells are produced.

Proliferate  then differentiate

1. Time lag

2. Antibodies produced, appear the same

3. Balanced of antibodies circulating  may be responsible to increase the

speed of immune response  speed up recognition by memory cells and
TH cells (presentation of antigen is shorter  much more rapidly)

4. Plateau: Antigens are not cleared  antigens no longer present, decrease

in antibodies  therefore increase, decrease, increase and decrease again
(infection!) Only when antigens are cleared, presentation of antigens will
not occur, blah blah  no more proliferation of B cells


In order to have B cells proliferate, presentation of antigen to TH cells, bind to B

cells, release cytokines, proliferation start.

Antigens can be presented faster to TH cells  produce antibodies faster

Large pool of memory cells remaining in the blood  initially, very small amount
of naïve B cells  each naïve B cells can produce ten thousands antibodies 
each naïve B cells proliferate  effect is multiplied many times  due to larger
pool of memory cells due to first exposure of antigens

Concentration of antibodies produced increased many folds.

Cytokines responsible for: Cell division and differentiation of B cells  B plasma

cells (lifespan of about 3 days)

No more antigens  Stop division of plasma cells to give antibodies


Memory cells circulate through the blood, lymph and tissues, probably not manufacturing
antibodies (Perelson et al., 1978), but when exposed to a second antigenic stimulus
commence differentiating into large lymphocytes capable of producing high affinity
antibody, preselected for the specific antigen that had stimulated the primary response.