indicate a need for further rationalising the provision and distribution of special care baby units. The case for this is further strengthened by our other findings. Even in the three well-endowed regions in this study it has not proved possible to staff and equip all officially recognised units to the standard recommended by the expert group. Moreover, since the group's report was published, increasing technological requirements together with inflation have made it a continuing struggle to maintain the standard of excellence required of the few units that provide intensive care for the illest babies. A further argument for rationalisation is the demonstration by Blake et a19 of the successful results of transporting sick babies when this is well organised by the intensive care nursery that is to receive the babies. Any replanning of nurseries must, however, take into account References

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SUMMARYThe mechanism by which specific immunotherapy exerts its beneficial effect remains unclear. In order to evaluate the influence of venom immunotherapy on the T-cell cytokine pattern of allergic reactions, we studied interleukin-4 (IL-4) and interferon-g (IFN-g) mRNA expression of peripheral T lymphocytes from 12 patients undergoing rush venom desensitization, before treatment at Day 0 (D0), at Day 15 (D15) and Day 90 (D90) after treatment, and from seven controls. Antigen-specific T-cell proliferation was also determined. Cytokine mRNA expression was evaluated using in situ hybridization, 24 hr after culture of peripheral T cells with medium, venom, or an unrelated allergen. Allergen-induced T-cell proliferation decreased at D15 and D90 of rush immunotherapy (P 4 0 . 02). In venom-stimulated cultures of the patient group, there was a decrease in IL-4 mRNA-positive cells at D15 and D90 (P 4 0 . 001). Before desensitization, IFN-g mRNA expression was lower in patients than in controls and did not increase after in vitro allergen stimulation. In contrast, after immunotherapy, spontaneous IFN-g mRNA expression increased, but only at D90 (P 4 0 . 001). The cytokine pattern observed at D90 after immunotherapy was similar to that observed in control subjects. In conclusion, venom immunotherapy induced an altered cytokine mRNA pattern in allergen-stimulated T cells which was dissociated from the early changes of allergen-induced T-cell responsiveness.

Immunity to schistosomes, helminth worms that infect 200 million people, is targeted to invading larvae (concomitant immunity). In vitro studies have revealed the role of T cells and of particular antibody isotypes in immune defense: IgE antibody cooperates with mononuclear phagocytes, eosinophils, and platelets to kill schistosome larvae. IgE antibody appears as an essential component of acquired resistance in rats. The role of IgE antibody has recently been confirmed by epidemiological studies demonstrating a positive correlation between the acquisition of resistance to reinfection by schistosomes and the level of IgE antibody to the parasite. A negative correlation found in these studies with the levels of IgM, IgG2, or IgG4 antibodies could be related to the development of a blocking antibody response. Antigens involved in protective immunity are expressed transiently at the surface of schistosomes. Sm28, a glutathione-S-transferase, induces significant protection against schistosome infection in rodents and nonhuman primates. In addition, this vaccine reduces the size of egg granulomas and egg output. Besides allowing the definition of a vaccine strategy against a major disease, studies on immunology of schistosomiasis have unraveled unsuspected antigenic mimicry between schistosomes and HIV regulatory proteins and have led to the demonstration that IgE antibody, a protective isotype against helminths, may also activate Fc epsilon-RII-bearing mononuclear phagocytes, eosinophils, and platelets in allergic disease.

Allograft recipients undergoing cytomegalovirus infection present increased proportions of circulating CD8+ lymphocytes. A longitudinal study of 11 kidney and five liver allograft recipients with primary CMV infection but no other etiological factor of graft dysfunction revealed selective imbalances of peripheral blood CD8+ T cell subsets. Initially, CMV viraemia is associated with elevated CD8+bright T cell numbers and T cell activation. Activation markers fall to normal when viral cultures become negative (before the end of the first month). During the second to sixth month, most (12/16) patients keep up high CD8+ T cell counts (1050-2900 CD8+ cells/mm3), comprising an uncommon CD8+ T cell subset, as 45-73% of CD8+bright lymphocytes were CD3+ and TCR alpha beta+, but were not stained by anti-CD28, CD11b, CD16, CD56, and CD57 antibody. Unexpectedly, CD8+CD57+ T cells, a hallmark of CMV infection, do not appear until the second to sixth month of primary CMV infection, and their numbers increase progressively thereafter. They become the predominant CD8+ T cell subset after 6 months of infection and their persistence for several (up to 4) years is strongly correlated (r = 0.87) with expansion of CD8+ cells. By analysis with MoAbs, there was no bias towards the use of particular TCR-V beta gene families at any time of primary CMV infection. Persistence of CD8 lymphocytosis is thus directly related to the rate of expansion of an uncommon CD8+CD57- subset and its progressive replacement by CD8+CD57+ T cells that are chronically elicited by CMV.