title: An immunologic homunculus for type 1 diabetes.
abstract: Autoimmune diseases such as the diabetes that develops in NOD mice depend on immunologic recognition of specific autoantigens, but recognition can result in a pathogenic or protective T cell response. A study by Du et al. in this issue of the JCI demonstrates that TGF-beta signaling by T cells recognizing the insulin peptide B:9-23 is essential for such protection and that this inhibitory cytokine functions in both a paracrine and an autocrine manner (see the related article beginning on page 1360). We propose that the insulin peptide B:9-23 and a conserved TCR motif form an "immunologic homunculus" underlying the relatively common targeting of insulin by T cells that, as demonstrated by the study of Du and coworkers, results in a protective T cell response, or diabetes, as shown by other investigators, for related T cell receptors.
authors: Barbara Davis Center for Childhood Diabetes, University of Colorado at Denver and Health Sciences Center, Aurora, Colorado, USA.
authors: Dirk
authors: D
authors: Homann
authors: George S
authors: GS
authors: Eisenbarth