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CANCELLED. EGENIS seminar series: Dr Gregor Greslehner (University of Bordeaux/CNRS)

Egenis seminar series

May be rescheduled.

Event details

If correct, these molecular structures would be crucial for solving the riddle of how the immune system is able to distinguish between self and non-self – and between harmful and beneficial microorganisms.

However, this narrative faces a major challenge, as molecular motifs are being shared among pathogens and symbiotic commensals alike. Both express a similar set of molecular patterns that are specific for prokaryotes. Other instances are known in which one and the same molecular motif can trigger opposing immune reactions, depending on the presence or absence of additional signals in the cellular context. It is speculated that a second “danger” signal might be needed in order to trigger an immune response. Whatever the nature of this second signal might be, it will require stepping away from the fixation on molecular patterns. I argue that it is rather structural motifs of networks which carry the explanatory weight in these immunological processes. I suggest to distinguish between different meanings of ‘structure’ and ‘function’, to which separate explanatory roles can be attributed. While the three-dimensional shape of signature molecules (structure1) can be used to explain their function1 – understood as biochemical properties and activities – their immunological function2 – biological roles, like immunogenicity – can only be explained with respect to higher-level structures2, i.e. the interaction network of molecules and cells. These different explanatory roles also imply different explanatory accounts. The former remains within a physico-chemical framework, whereas the latter rather calls for mechanistic and topological explanations.

Studying the interaction topology and dynamics of structures2 with mathematical tools, e.g. modelled as signalling games, promises to shed new light on these interaction processes that increasingly get to be described as equilibrium states between multiple interaction partners by immunologists. Rather than focusing only on the presence or absence of molecular signatures, topological properties explain the features of these networks and their activities beyond the molecular interactions between PAMPs and PRRs. This way, opposing effects resulting from the same kind of molecular structure1 can be explained by differences in their “downstream” organisational structure2. While still preserving the centrality of structure-function relationships, I suggest to keep these conceptually different notions of ‘structure’ and ‘function’ and their respective explanatory roles apart.


Byrne House