Having read this review which I think is perfect, but I am not recognized as immunologist to make such estimations, I am even more convinced that late "Charly" Janeway was a real pioneer. I happily remember his visit at Stanford when he gave a talk in Irv Weissman's house with a huge dinner, a thrilling experience with so fascinating views and scientific as well as social anecdotes. But I guess, we should not only judge good scientist from the awards they received or not.
Article Innate immunity's path to the Nobel Prize 2011 and beyond
Absolutely! He totally deserved it. And Ruslan, whom he trained was very close to getting it but for politics...Anyway their work on pattern recognition receptor and innate immunity will always be a benchmark..prize or no prize, these scientists never worked to get these prizes for sure!
@Andrei Of course your logic about the "toll" (German word for "amazing", when Nüsslein-Vollhard saw in the 1980s some (non-immune) function of it in fruit flies) being before the "toll-like" is right. And also, the finding of the immune function in fruit flies in the 1990s was before the finding in mammals - this is what you probably meant.
On the other hand, according, for example, to the review mentioned in my question:
"The upregulation of costimulatory signals on DCs, induced by
postulated pathogen-associated molecular patterns (PAMPs), was
speculated by the late Charles Janeway [14] in 1989 to play an
essential role in alerting adaptive immunity [15]."
Some of the "theory" was before the findings... This reminds me to the fascinating theory by Stanley Prusiner on Prions who fighted mayby 30 years against the dogma of infectious agents need to have genes, like a virus or bacteria. He made the paradigm shift to his "protein only" theory, i.e. a protein can cause an infectious prion diseases like mad cow disease, Creutzfeld-Jakob and similar diseases. Prusiner did not even have to share his Nobel prize, although many others tried to proof the postulates, like Charles Weissmann and his group cloned the gene, did the K.O. in mice (with H.-R. Büehler) and showed that mice without the prion gene can not get infected (with A. Aguzzi), unless one re-introduces the prion gene as a transgene. So, here the theory or postulates were first, the proof of concept later. Is my logic too simple?
I recently had the chance to attend some Nobel lectures from Hoffmann last year and Nüsslein-Vollhard this year.
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