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Lecture 5

BIOL 103 Lecture Notes - Lecture 5: Human Leukocyte Antigen, Cytotoxic T Cell, Cell-Mediated Immunity

Course Code
BIOL 103
Virginia K Walker

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Gene assembly
Increased diversity
Novel joints – repetitive palindromic DNA, if those repeats were cut precisely in
the V region and matched the cut in the J region, it is a ‘perfect’ join / extra
repeat, adds one to a few amino acids to that region between the J and the V
region / lost one to a few amino acids on that chain
Add one to a few amino acids – adding variability
If these are overlapping, and we’ve lost some, this will be a little shorter
Tends to increase variability
Hyper mutation – enzyme which will dominate cytosine and this will have to be
repaired to a thymine – V*, increasing variability by creating mutations in that
variable area
Not all that important for us because we have so many variable regions
Chickens depend on this because they have few variable regions
Assembly of a light chain
Single stranded DNA? We have 2 chromosomes, why did we draw it as a single
DNA strand
Allelic exclusion – we have 2 chromosomes, and the first one assembled will be
used to make the light chain
Heavy chain
500 variable regions
2 different kinds of J regions, 2 assemblies, 2 loops
splicing  mRNA
In a particular immature B lymphocyte the 300th V region is join is joined to the 3rd J
region. Draw the primary transcript and show the processing involved to make a mature
mRNA corresponding to the light chain of the mature B lymphocyte.
We may need to recognize up to a million foreign antigens in our lifetime. How is this
There must be some king of interesting story during B-lymphocyte development that
explains this mystery
Immunological memory
Two lines of defence
B cellular immune response
plasma b cells secrete antibodies
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T lymphocytes
have t receptor – dimer
disulfide bride
variable regions and constant region
alpha chain, joining regions, C region
joining, splicing, alpha subunit
the variable is going to make a recognition for a foreign antigen
can also bind MHC protein
aka human leukocyte antigen (HLA)
having an MHC I requires a nucleus
T receptor binding to foreign antigen – binding is stabilized by CD4/CD8
Bind to foreign antigen and at the same time bind to MHC II
Pink thing in the middle – foreign antigen
Cell mediated immunity
Will take foreign invader in, lysosomes will fuse, cut it up, MHC will drag those
digested proteins to the surface and display them (foreign antigens)
MHC and antigen, all kinds of virgin T-cells, out of that whole population, only
one T will have a receptor which will recognize the foreign antigen
If it binds together, it is stabilized by a cluster determinate
Sets of cascade, cell wants to divide, and we get a huge population – memory
and helper T cells
4 functions
binds to apc
Helper T-cells are called T4
Clonal population – all of these receptors recognize this particular antigen
Binds T-cell
T-cells are like politicians telling kernels what to do
Helper T cells will mobilize killer T-cells
Being infected by foreign antigen
Recognize both ^^
Allows killer T-cell to make perforin
Will insert pore and kill cell
Helper T-cells allow production of more killer T-cells
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Killer T-cells – not long lived in the body
Platelets can influence positive feedback system to T-cells and keep them active
Calcium helps put the pore into the cells
Immune tolerance
Why won’t our own antibodies attack our own cells
T-cells maturing in thymus, if they detect any self-antigen, those T-cells will die if
they bind
Clonal inactivation – never express T-cell receptors that cross react to our own
Can go wrong
Autoimmune diseases – multiple sclerosis – immune system attacks myelin, need
fast signals to speak and move around – T-cell mediated attack – may have
succumb to viral infection with sequence that looks like myelin – there is a
response to get rid of virus, and real myelin gets attacked too
Myasthenia gravis – antibodies attack post-synaptic membrane
RA – joints attacked
T1D – because of viral infection
HD – thyroid
Epitotes look similar to our own antigens – we could treat symptoms or suppress
immune system
Anti-cancer agents inhibit mitosis
Not enough of a good thing
Not enough B-cells – no agglutination
Don’t die right away because of passive immunity
Anti-bodies in moms circulation
Placenta has XC receptors
Can take up antibodies from moms circulation
Babies take up antibodies, and baby can be immunized
Once baby is born – digestive cells in baby for weeks after birth can also take up
antibodies (receptors in intestinal cells) – evolved so that mothers milk can
contain antibodies and protect baby after birth – newborns vulnerable to
By 6 months, these antibodies have disappeared from baby
Absence of functional T cells
undeveloped thymus, cant produce T-cells
no B cells and no T cells
eg. Boy lives in bubble, died from infection of bone marrow transplant
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