The mesenteric lymph nodes and Peyer's patches of the small bowel present a significant target for immune attack in rejection. In addition they have the potential to proliferate and cause graft-versus-host disease (GVHD). Immune-mediated impairment of mucosal barrier function will allow translocation of bacteria from the gut lumen into the blood stream. This factor, with the development of septicaemia, was probably responsible for the majority of deaths in early clinical cases treated with azathioprine and prednisolone. In the experimental situation GVHD and rejection can be studied as separate entities in transplants between parental strain rats and F1 hybrids. The use of immunohistochemical staining with strain specific monoclonal antibodies has enabled the migration pattern of lymphocytes to be studied. Within 24 h of transplantation donor lymphocytes can be detected in the spleen and mesenteric lymph nodes of the recipient. This cell transfer is clearly effected through the blood stream as the severed lymphatics of the grafted bowel take at least 7-10 days to regenerate and from connections with the recipient lymph system. At a practical level impairment of normal lymphatic drainage may cause problems with the absorption of fats and fat-soluble molecules such as cyclosporin. Denervation of the bowel also presents a problem in the initial phase after transplantation, with hypersecretion from the crypts causing diarrhoea. Since the introduction of cyclosporin a small number of successful human transplants have been reported.(ABSTRACT TRUNCATED AT 250 WORDS)