To second this point, since the goal is to understand the "natural states" that T cells can adopt in various environmental conditions, profiling KO T cells are out of scope per se. But if a genetically engineered mouse serves as a disease model, particularly if the mutation is extrinsic to T cells, then it is within the scope of the ImmGen T project.
Interesting suggestion, raises the question of KO mice within immgenT.
Since the scope of the project is to profile "all the states that T cells can adopt", transcription factor knockouts that artificially perturb the transcriptional regulatory network would not belong (don't think that we should include Tbet knockouts, for instance).
But here the situation is different. If I understand what you are suggesting, would not aim to analyze the artificifial "wannabe Tregs*" , but the FoxP3-negative conventional T cells that respond in the autoimmune context of a Treg deficiency (in addition, it is a model for the human IPEX disease)
So let's do it !
* of Rudensky/Chatila fame (messed up cells that have many characteristics of Tregs but lack FoxP3)
To second this point, since the goal is to understand the "natural states" that T cells can adopt in various environmental conditions, profiling KO T cells are out of scope per se. But if a genetically engineered mouse serves as a disease model, particularly if the mutation is extrinsic to T cells, then it is within the scope of the ImmGen T project.
Interesting suggestion, raises the question of KO mice within immgenT.
Since the scope of the project is to profile "all the states that T cells can adopt", transcription factor knockouts that artificially perturb the transcriptional regulatory network would not belong (don't think that we should include Tbet knockouts, for instance).
But here the situation is different. If I understand what you are suggesting, would not aim to analyze the artificifial "wannabe Tregs*" , but the FoxP3-negative conventional T cells that respond in the autoimmune context of a Treg deficiency (in addition, it is a model for the human IPEX disease)
So let's do it !
* of Rudensky/Chatila fame (messed up cells that have many characteristics of Tregs but lack FoxP3)