1cii) Yeah that should be okay
2c) The main point about the tertiary structure is that it's the overall 3-d conformation of the protein due to a variety of intermolecular interactions which largely determines its function, so I think you've got it there.
3ii) That's valid.
5b) Hm.. not too sure about this one. Your reasoning is sound, but the fact that they specifically refer to the autoimmune disease as eliciting antibody production implies that this is a humoral response, not a cell-mediated one.
9b) That's alright because you mention their respective alleles
With regards to genetic drift/bottleneck effect, your definitions are okay; if they're merely worded differently then that's no problem.
Thank you man, means a lot.
As for the 5b question, my answer could be partially correct but I just realised also that autoimmune disease certainly do involve the recognition of self cells as non-self, but this does not necessarily mean that ONLY cell-mediated immunity responds. Clearly as I just discovered over some research too, that Cytotoxic T cells can destroy the targeted cells via recognition of the self antigens presented on MHC I markers as non-self, OR the production of autoantibodies that agglutinate the self cells/tissue. This is all possible because of the activated T helper cells, which in turn release cytokines to activate BOTH cytotoxic and B cells.
However, this raises another issue at hand. During transplant rejection, why is it that only the cell-mediated response occurs? Why cannot antibodies be produced to agglutinate the non-self cells? Like sure there's non-self antigens presented on the MHC I of the organ transplant, but wouldn't the T helper cells be activated either way, and thus activate B and T cells?