Class Notes (1,100,000)
CA (650,000)
UTSG (50,000)
IMM (200)
IMM250H1 (200)
Lecture

Notes taken during lecture


Department
Immunology
Course Code
IMM250H1
Professor
J.Gommerman

This preview shows pages 1-2. to view the full 7 pages of the document.
LECTURE – Feb. 15/2011
T-Cells
Midterm – approximately 2 hours, all Multiple choice questions
Results will be posted before drop date
March 1st material not covered on midterm
T-cell – triggered by antigen how?
Adaptive immunity requires recognition of antigen; takes longer to develop, days to weeks;
Can recognize 10 billion antigen specificities – due to random rearrangement
process in bone marrow at DVJ locus
Highly variable immune system – can recognize just about anything and
everything
Can improve as the response progresses
TWO major subsets of lymphocytes – B and T
oB secrete antibodies – which have same specificity as B cell receptor
displayed on surface of B cell
oT lymphocytes – expand and become effector T cells
Debate whether humoral or cellular immunity is more important
Cellular response – T cell response helped by dendritic cells
NaΓ―ve recipient – someone who has never seen the infection before
Ex. response to TB – cannot transfer TB immunity with only serum
Innate immune response – does not work by clonal selection – β€œdumb” immunity –
everybody responses and responses the same way – but adaptive is more selective
Adaptive immune responses
Specific
Diversity
Memory
Self/non-self discrimination
oAutoimmunity – when own cells attacked by adaptive immune system
Know when to wind down – do not want it to be on all the time
KNOW THESE HALLMARKS
Antigens
Displayed by pathogens
Recognized by adaptive immune system
Other potential antigens include self antigens, tumour antigens, transplanted
tissue
See portion of bacteria, called epitope
www.notesolution.com

Only pages 1-2 are available for preview. Some parts have been intentionally blurred.

Ex. have TB, will have antibodies to different antigens on different parts of TB
This is the polyclonal response
Polio virus
Three different proteins on the coat
Epitopes are what are seen
Proteins are made – only small percentage of genome codes for proteins
Linear epitope – runs length of linear protein (before folding)
Conformational epitope – seen once the protein is folded
B-cells typically see conformational epitopes
T-cells see antigens differently, CAN see linear epitopes
oBut proteins don’t exist in linear form…
Influenza mutates year to year
Most mutated proteins are the ones on the surface of the virus particle
T-cell receptors recognize receptors within the coat, those epitopes more
conserved because they typically are crucial for viral replication, etc.
Not foolproof but less susceptible to drift than B-cell epitoptes
 Denatured proteins recognized by T-cell receptors
oPeptide antigens recognized
oPeptides are fragments of amino acids
oPeptides made inside infected cell, loaded onto MHC
Cell infected by virus –
Peptide must be seen in context of MHC – so can respond to pathogen
T-cell expands and makes daughter cells
Summary
T-cells activated by only protein antigens and recgonize peptides only
T-cells recognize only linear peptides
Only one unique t-cell receptor
oSeveral copies of this receptor displayed on surface of cell
PART 2: How T-cell receptor is diverse enough to see so many diff antigens
RANDOM process – takes place in bone marrow
Genes code for t-cell receptor – locus of genes called T-cell locus receptor
Alpha locus – DJ; beta locus – VDJ
VDJ recombination
T-cell receptor
Diversity of which VDJ genes selected and put together
More diversity from putting together the alpha and beta chains
T-cell receptor never secreted, stay on t-cell surface always
www.notesolution.com
You're Reading a Preview

Unlock to view full version