Journal Watch: MHC and intracellular self

Shiv Prasad shiv at
Wed Aug 19 15:19:32 EST 1992

In article <92232.101920FORSDYKE at QUCDN.QueensU.CA> <FORSDYKE at QUCDN.QueensU.CA> writes:
>  Forsdyke: Yes, synthesis and degradation (turnover).  OK. Now be patient and
>            tell me what determines rates of synthesis and degradation.
Ok, rates of transcription and translation determine synthesis (I hope we're
not going to get into promoters and enhancers).  As far as degredation, protein
stability, i.e. maintaining it's conformation, is certainly a factor, as de-
natured proteins may be degraded, but I'm not really sure what controls the 
half-lives of proteins.  I'm not exactly sure where you're going with this.
Are you going to suggest that viral proteins have longer half-lives, which may
lead to higher relative concentrations in the cell?
>  Forsdyke: OK. Let's just take a "generic" virus which goes about its
>            business within the cell and eventually lyses the cell.
>            It will make some viral proteins more than others, but a minimum
>            of one protein would be     necessary in order to get a foreign
>            peptide displayed at the cell surface with MHC class I.

So back to the original question, what is the system that prevents all of
the cellular self-proteins from competing with the viral non-self protein.

>>>References:   Forsdyke, D. (1992) Bionet.immunology 812 947edt
>>>              Prasad, S. (1992) Bionet.immunology 814 1516gmt
>>>              Forsdyke, D. (1992) Bionet.immunology 817 1757edt
>>>              Prasad, S. (1992) Bionet.immunology 818 133gmt
>>               Forsdyke, D. (1992) Bionet.immunology 818, 1616edt
>                Prasad, S. (1992) Bionet.immunology 819, 405gmt

P.S.  How are we doing on the citation indices :-).

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