T-Lymphocyte Migration is Differently Regulated in Appendiceal Lymph Follicles and Intestinal Peyer’s Patches

The appendix was long considered a redundant organ. However, thereafter, analysis of immune components of the appendix revealed that slightly fewer than one third of its cells are T cells and that normal adult appendiceal lymphocyte reactivity is predominated by helper T cells [1]. In addition, the appendix has been reported to be involved in intestinal inflammation. For example,“skip lesions”of the appendix were detected in ulcerative colitis (UC) specimens examined [2], and discontinuous appendiceal involvement was found in patients undergoing proctocolectomy for UC [3]. As regards the mechanisms in appendiceal inflammation, Bittinger et al. demonstrated a different expression of cell adhesion molecules by endothelial (EC) and mesothelial cells (MC) in the various stages of appendicitis, with early Eselectin and intercellular cell adhesion molecule-1 (ICAM-1) expression in EC, followed by vascular cell adhesion molecule (VCAM-1) in EC and MC [4], suggesting that adhesion molecules play pivotal roles in appendiceal inflammation. In addition, recently, potential roles of chemokines and their receptors in lymphocyte migration have been reported. On the other hand, preventive effects of appendectomy for UC have been reported in a clinical setting [5–8]. Moreover, in an experimental model of young T-cell receptor (TCR)-a deficient mice, removal of the appendix inhibited the induction of experimental colitis [9]. In another experimental model