ONLINE COVER Spontaneous Eosinophilic Esophagitis in Mice. This month’s cover shows esophageal cross-sections from 24-week-old mice stained with hematoxylin and eosin (left side) or an immunoperoxidase stain for the eosinophil granule protein major basic protein (right side). Laky et al. found that knock-in mice heterozygous for a loss-of-function M318R mutation in TGFβR1 identified in atopic patients (designated as R1 mice) show esophageal dilation and intense inflammation—including many eosinophils within the epithelial layer—compared to wild-type mice. These features meet the criteria for a histologic diagnosis of eosinophilic esophagitis. The spontaneous phenotype of these mice was also observed in lymphocyte deficient Rag2 knockout mice, pointing to the key role TGFβ signaling plays as a regulator of localized allergic inflammation in the esophagus.
Credit: Karen Laky/NIH/NIAIDONLINE COVER Spontaneous Eosinophilic Esophagitis in Mice. This month’s cover shows esophageal cross-sections from 24-week-old mice stained with hematoxylin and eosin (left side) or an immunoperoxidase stain for the eosinophil granule protein major basic protein (right side). Laky et al. found that knock-in mice heterozygous for a loss-of-function M318R mutation in TGFβR1 identified in atopic patients (designated as R1 mice) show esophageal dilation and intense inflammation—including many eosinophils within the epithelial layer—compared to wild-type mice. These features meet the criteria for a histologic diagnosis of eosinophilic esophagitis. The spontaneous phenotype of these mice was also observed in lymphocyte deficient Rag2 knockout mice, pointing to the key role TGFβ signaling plays as a regulator of localized allergic inflammation in the esophagus.
Credit: Karen Laky/NIH/NIAID