Autocrine DNA fragmentation of intra-epithelial lymphocytes (IELs) in mouse small intestine.

Intraepithelial lymphocytes (IELs) are present in the intestinal epithelium. Mechanisms of IELs for the protection of villi from foreign antigens and from infections by micro-organisms have not been sufficiently explained. Although more than 70% of mouse duodenal and jejunal IELs bear γδTCR (γδIELs), the functions of γδIELs are little investigated.

Activation of intra-epithelial lymphocytes; their morphology, marker expression and ultimate fate.

Intraepithelial lymphocytes (IELs) have been considered to play a key role in the defense system of the small intestine. Its mechanism has not been made sufficiently clear. Studies on IELs have been extremely limited to functions of αβ T-cell receptor (αβTCR) IELs (αβ-IELs).

Granzyme B-dependent and perforin-independent DNA fragmentation in intestinal epithelial cells induced by anti-CD3 mAb-activated intra-epithelial lymphocytes.

We previously found that an i.p. injection of anti-CD3 monoclonal antibody (mAb) into mice caused DNA fragmentation in the intestinal villous epithelial cells (IVECs) of the duodenum and the jejunum.

DNA repair after DNA fragmentation in mouse small intestinal epithelial cells.

In our earlier work, we found that, in mice, i.p. injection of anti-CD3 monoclonal antibody activated intraepithelial lymphocytes (iIEL), leading to DNA fragmentation in villous epithelial cells of the duodenum and jejunum within 30 min.

The effect of high strength static magnetic fields and ionizing radiation on gene expression and DNA damage in Caenorhabditis elegans.

Magnetic resonance imaging with high static magnetic fields (SMFs) has become widely used for medical imaging purposes because SMFs cause fewer genotoxic side effects than ionizing radiation (IR). However, the effect of exposure to high SMFs on global transcription is little understood. We demonstrate that genes involved in motor activity, actin binding, cell adhesion, and cuticles are transiently and specifically induced following exposure to 3 or 5 T SMF in the experimental model metazoan Caenorhabditis elegans.