Dr. Murai Éva szerk.: Parasitologia Hungarica 22. (Budapest, 1989)

mast cell accumulation and worm loss or damage, (b) study of the effect of mast cell mediators on worm survival, (c) examination of parasite establishment and survival in animals treated by mast cell mediator antagonists, (d) use of animal hosts deficient in mast cells and other immune components (LEE, SWIETER and BEFUS 1986). Ad a

) Although mast cells have been suggested to be major effector cells in the immune response to helminths, it is not always possible to correlate mast cell responses with worm expulsion. This may reflect lack of correlation, and, partly at least, might be explained by technical reasons. In the rat two major mast cell subsets, connective tissue mast cells (CTMS) and mucosal mast cells (MMC) have been Identified. It has become known recently that the classical histochemical methods for staining mast cells in histological sections, which are based on the detection of mast cell granule glycosaminoglycans (GAG), such as the Alcian blue/safranin staining techniaue, are unlikely to provide a reliable phenotypic identification of mast cells. Recent experiments offer an alternative and more effective approach based on the determination of the chymotrypsin-like enzymes: rat mast cell proteinases I and II (RMCPI and RMCPII) (WOODBURY et al. 1978; KING and MILLER 1984; GIBSON and MILLER 1986; GIBSON et al. 1987). Using a recently developed immunohistochemical technique and paraformaldehyde fixation, it was possible to demonstrate that CTMSs and MMCs can readily be distinguished by their RMCPI and RMCPII content, respectively. This suggests that granule proteinase phenotyping may provide a promising technique In studies of mast cell heterogeneity and functions. This method can be applied to measure the concentration of mast cell proteinases also in tissue homogenates and the blood. The spectrum of activity of mast cell proteinases awaits clarification. It Is known, however, that RMCPII plays an Important role in the generation of intestinal anaphylactic reaction (KING and MILLER 1984), and that RMCPII levels appear to show good correlation with worm expulsion even when the histological picture does not (WOODBURY et al. 1984). A similar pattern of the release into the gastric lymph of sheep mast cell proteinase (SMCP) following oral challenge of immune sheep with 50 000 Ostertagia circumctncta L

3 has also been demonstrated (MILLER 1987; HUNTLEY et al. 1987). Recent evidence suggests that mast cells of different phenotypes are selectively recruited to some parasite induced lesions, which implies variations also in their respective activities (CHERNIN et al. 1988). A causal association between mucosal mastocytosis and the expulsion of intestinal nematodes has long been suspected although it is clear now that immune rejection of worms can take place also in the absence of demonstrable MMC accumulation. Thus the basis of this association remains to be Identified. In recent studies of DEHLAWI, WAKELIN and BEHNKE (1987) it was found that the nematode Nematospiroides dubius in mice actively depresses the potential of the host for expression of a MMC response and is capable of persisting for up to 8 months. Infection with N. dubius can prevent or delay also the MMC response elicited by concurrent or subsequent infection with T. spiralis and N. brasillensis. It is of special Interest that SJL mice expel also primary Infections with N. dubius, however, worm expulsion Is not accompanied by mastocytosis. LOSSON, LLOYD and SOULSBY (1985) demonstrated that the depression of immune responsiveness is induced by larval stages of N. dubius, and develops very early during infection when little damages have been apparent in the intestinal mucosa. Ad b) It is known from in vitro studies that although mast cells adhere to the cuticle of Intestinal nematodes, they do not kill them. Mast cells exert their effects on surrounding tissues by a wide range of chemical mediators which are released upon activation. There are