Open AccessOdDHL Inhibits T Cell Subset Differentiation and Delays Diabetes Onset in NOD Mice
Author(s) -
Wendy Gaisford,
David Pritchard,
Anne Cooke
Publication year - 2011
Publication title -
clinical and vaccine immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.649
H-Index - 77
eISSN - 1556-6811
pISSN - 1556-679X
DOI - 10.1128/cvi.00032-11
Subject(s) - nod , autoimmunity , immunology , immune system , autoimmune disease , nod mice , biology , t cell , quorum sensing , cell , pseudomonas aeruginosa , cellular differentiation , microbiology and biotechnology , diabetes mellitus , antibody , genetics , endocrinology , bacteria , gene , biofilm
Some infectious diseases have been shown to halt the onset of autoimmune disease in animal models and have been suggested to also influence autoimmune pathology in humans. The isolation and study of small molecules and proteins from the infectious agents responsible for the protective effect will enable a mechanistic understanding of how these components may prevent or delay the onset of autoimmunity. In this study we confirm that the quorum-sensing signal molecule OdDHL from Pseudomonas aeruginosa can delay the onset of type 1 diabetes in the NOD mouse model. Furthermore, using an antigen-presenting cell-free system, we find not only that OdDHL inhibits the proliferation of naïve T cells but also that it directly inhibits the differentiation of T cell subsets. OdDHL was shown to have no effect on the inhibition of primed and committed differentiated T cell responses, suggesting that that immune mechanism mediated by this molecule may be more restricted to initial stages of infection.