I have a question about the epitope GP33 of LCMV. In some paper, it is indicated that the wild type GP33-41 is KAVYNFATM, yet in others, the wild type GP33-41 turned to be KAVYNFATC. Which one is the right one?
Is it because the two different wild type GP33 are from different substrain of LCMV?
Hi. The wildtype sequence is KAVYNFATC. In the past it has been show, if the C is mutated to M you will raise affinity for MHC, therby stabilizing the responses.
Just some examples for the "m" variant.
Functional management of an antiviral cytotoxic T-cell response.
Bachmann MF, Speiser DE, Ohashi PS
J Virol. 1997 Aug; 71(8):5764-8.
Original antigenic sin impairs cytotoxic T lymphocyte responses to viruses bearing variant epitopes.
Klenerman P, Zinkernagel RM
Nature. 1998 Jul 30; 394(6692):482-5.
Viral escape at the molecular level explained by quantitative T-cell receptor/peptide/MHC interactions and the crystal structure of a peptide/MHC complex.
Tissot AC, Ciatto C, Mittl PR, Grütter MG, Plückthun A
J Mol Biol. 2000 Sep 29; 302(4):873-85.
Hi Dr. Lehmann, thank you for helping me clarify this point. On more question, is there any difference between the immune responses targeting two different GP33? Would different affinities lead to different CTL responses?
Oh, sorry, i should read those papers first before I ask.
Two my knowledge, the "kind" of immune response should be the same, but I think the strenght of response will be better with the "mutated" epitope.
but I have never compared it by myself (I'm sure there is data in the primary literature developing this mutated form of this CD8 epitope).
Hi Dr. Lehmann, I agree, the strength of response will be different. Yet I also find a paper (1), it shows the High-affinity of GP33 C8M - MHC/TCR interaction overcomes the lack of CD8 engagement in vitro, in terms of the CTL and T cell proliferation. It indicates the stimulation of T cells can be CD8 independent. Would that change partly the immune response not only on strength but on the type?
1 Samantha E,Kerry, et al. Interplay between TCR affinity and necessity of coreceptor ligation: high-affinity peptide-MHC/TCR interaction overcomes Lack of CD8 engagement. the Journal of immunology. 2003
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