Food allergy is a major public health problem. Studies have shown that long-term interactions between activated leucocyte cell adhesion molecule (ALCAM/CD166) on the surface of antigen-presenting cells, and CD6, a co-stimulatory molecule, influence immune responses. However, there are currently no studies on the functions of ALCAM in food allergy. Therefore, we aimed to identify the functions of ALCAM in ovalbumin (OVA)-induced food allergy using ALCAM-deficient mice. Wild-type (WT) and ALCAM-deficient (ALCAM ) mice were sensitized intraperitoneally and with orally fed OVA. The mice were killed, and parameters related to food allergy and T helper type 2 (Th2) immune responses were analysed. ALCAM serum levels increased and mRNA expression decreased in OVA-challenged WT mice. Serum immunoglobulin (Ig)E levels, Th2 cytokine mRNA and histological injuries were higher in OVA-challenged WT mice than in control mice, and these were attenuated in ALCAM mice. T cell proliferation of total cells, CD3 CD4 T cells and activated T cells in immune tissues were diminished in OVA-challenged ALCAM mice. Proliferation of co-cultured T cells and dendritic cells (DCs) was decreased by the anti-CD6 antibody. In addition, WT mice sensitized by adoptive transfer of OVA-pulsed ALCAM BM-derived DCs showed reduced immune responses. Lastly, serum ALCAM levels were higher in children with food allergy than in control subjects. In this study, serum levels of ALCAM were elevated in food allergy-induced WT mice and children with food allergy. Moreover, immune responses and T cell activation were attenuated in OVA-challenged ALCAM mice. These results indicate that ALCAM regulates food allergy by affecting T cell activation.

Mitochondria offer their energy for surviving [1] and control death or life [2]. Recently, it was reported that mitochondria and calcium ion could regulate their death and alive, too [3], [4]. The transfer of calcium from the ER to mitochondria, mitochondrial calcium uptake, and the consequence of cell death have drawn much attention in the structurefunction relation studies. C2-ceramide has been known a drug to induce cell death through mitochondria and calcium [5]. The present study has been attempted to reveal the ultrastructural changes that occur during induced apoptosis in HeLa cells when combined with ceramide. The functional importance of calcium transfer from the ER to mitochondria and on the consequence for cell death in those cells will be discussed. In this study, HeLa cells were induced cell death by C2-ceramide and rapid freezing. Then the calcium ion distribution in HeLa cell was detected by ToF-SIMS.