Tue Dec 7 12:11:18 EST 1993

Yes, the recent findings on IL-2 have given us much to think about. Ken
Frauwith and anyone else - you offer the much overused redundancy argument:
that is, if IL-2 knockouts don't behave as we would predict, then some other
mechanism must be compensating. While this argument may be insightful, it
could just be handwaving unless you propose some other mechanism. It was
interesting to note in the literature earlier this year (Cell, V73, pp147-57)
that human XSCID diease maps to the IL-2R gamma gene, and mutations at this
locus were found in these patients. Thus, humans with defective IL-2 signaling
can be immunodeficient. Although the murine knockouts were of different genes,
either IL-2 is functioning in ways other than we have previously thought, or
human and murine IL-2 are not entirely functionally homologous. ANY COMMENTS?

brett at borcim.wustl.edu

More information about the Immuno mailing list

Send comments to us at biosci-help [At] net.bio.net