A Proposed model of bacterial regulation of T1D. Type 1 diabetes is due to the acquisition of diabetogenic effector functions by prediabetogenic T lymphocytes (T lymphocytes which bear TCR specific for pancreas related antigens have not yet been activated). Gut flora has been shown to play a critical role in immune homeostasis (see text). In this model we propose that specific microbial strains such as L. johnsonii and SFB, which naturally reside within the mucosa, can inhibit the onset of T1D by inhibiting the development of diabetogenic effector functions by T lymphocytes. While IFNγ has been associated with effector functions which lead to T1D, the work by us and others has implicated that IL17 production by T lymphocytes is associated with effector functions that are protective in T1D.
