Free submandibular gland autotransplantation is used to treat absolute tear deficiency. Although disconnected from any peripheral innervation, most transplants show increasing secretion for years. We have evaluated the secretory activity and autonomic innervation of such transplants. Secretory activity of glands in response to parasympatholytics and parasympathomimetics was evaluated by Schirmer's test and Technetium scintigraphy. Submandibular gland tissue specimens taken before and after transplantation were examined histologically. Relative hypersecretion during the first postoperative week suddenly decreased but then slowly increased during the first postoperative year. Hypersecretion was significantly reduced by parasympatholytics while carbachol rapidly increased secretion. Histology of transplanted glandular tissue showed parenchymal atrophy. Cholinesterase-positive nerves were abundant and in a similar distribution to normal with scattered positive ganglion cells. Adrenergic axons were fewer than normal and irregularly distributed. Early hypersecretion may be due to release of neurotransmitters from degenerating terminal axons. This is followed by a period of minimal secretion during which hypersensitivity of acinar cells develops. With spontaneous reinnervation, secretion is accentuated by external sympathetic vasomotor adrenergic drive. This shows that submandibular glands can remain viable despite complete separation from their normal nerve supply and are capable of regaining a substantial secretory activity for years.

Activated T cells, with their secretion of cytokines, probably play an important role in the pathogenesis of mucosal lesions in coeliac disease (COD) and the prominence of a T-helper (Th)1-type cytokine pattern has been reported. As the process of immunological activation in the jejunal mucosa in active CoD has been shown to also cause some differences in peripheral blood lymphocyte populations, we sought to establish any changes in the Th 1/Th2 balance in peripheral blood of patients, at different stages of CoD, relative to healthy individuals. Twenty-two CoD patients and 10 healthy controls were included in the study. The Th1/Th2 balance was examined both in resting cells and after polyclonal stimulation using two different methods: intracytoplasmic cytokine contents were measured using an intracellular staining method and three-colour flow cytometry and cytokine contents of cell culture supernatants were measured using traditional enzyme-linked immunosorbent assays (ELISAs). Interferon-gamma (IFN-gamma)-producing cells (Thl) were as prominent in untreated CoD patients and treated CoD patients as in healthy controls, while cells fitting a Th2 or ThO-type cytokine pattern were few in all groups. In ELISA assays, Th1 type (IFN-gamma or interleukin (IL)-2) cytokines were again prominent in all study groups but no statistically significant differences were found in IFN-gamma, IL-4 or IL-2 levels among the three groups. These results suggest that the increased shift towards a Th1 response is mainly restricted to the actual site of inflammation and that circulating T cells do not show a similar response, presumably because activated cells in peripheral blood are too few. Further research on cytokine profiles measuring T-cell activation in CoD should be focused on the actual tissue of inflammation.

Reviews of French-Canadian books published in 1943.

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