After reading and rereading Patel et al, I'm not convinced that they
chose their STE2 and STE3 so carelessly. They were examining more than
100 surface molecules and just coincidently picked alpha-numeric symbols
that have been traditional and specific for many years; but perhaps that is
what they did.
My hypothesis is not dependent upon STE2 and STE3, but is primarily based
upon immunological cells within the nasal mucosa -- which, to my
knowledge, has not yet been researched.
If it turns out that Patel et al's STE2 and STE3 have zero homology with
yeast molecules of similar alpha-numeric nomenclature, I will conclude
that the Internet has in fact performed a useful function -- ie, that of
pointing out a flaw prior to hundreds of thousands of dollars poured down
yet another lab's drains.
In trying to pin down the STE2,3 ambiguity, I have written to the Patel
et al corresponding author.
I can't help but wonder, given the long-standing tradition of using ste2
and ste3 in reference to S. Cerevisiae receptors, why would researchers
and reviewers allow such a similar term to be used for molecules found in
the human thymic epithelium?
Regarding anecdotal evidence, you seem to have taken that notion out of
its context wherein Wedekind et al MHC data and other immune-related data
were cited. Often in human research, anecdotal data and hypotheses
derived therefrom help to guide what become actual collectings of data,
testing of hypotheses. For the record, the seemingly higher than
average presence of autoimmune dysregulations among HM was in fact first
pointed out to me by several HM themselves. Certainly, their impression
may be a "false positive", but at least one that is consistent with
MHC-related processes of human interactions as documented by Wedekind et al,
Blanchard et al, and others cited previously in this thread.
But thanks for making effort to address my hypothesis, including its
portion based upon ste2 and ste3 and Patel et al.
Teresa
