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SUMMARY In a group of 46 patients with retinitis pigmentosa (RP) we studied the presence of circulating immune complexes (CIC) and the alterations in the complement system. Our results showed the presence of CIC in 43.5% of the patients studied, reduced levels of the complement components C3 and C4 (p<0-001), and of the haemolytic activity CH50 (p<0-001) when compared with a control group consisting of a 100 healthy subjects. We found a statistically significant correlation between the values of C3 and CIC (p<0-01), C4 and CIC (p<0.01), and between CH50 and CIC (p<0-001). These findings indicate that the CIC may play a role in the pathogenesis of primary retinitis pigmentosa.

SUMMARYAdenosine deaminase (ADA) expression on the surface of mitogen-stimulated lymphocytes was studied by flow cytometry. The gate for lymphocytes was located by cell size (forward scatter), cytoplasmic complexity (side scatter) and by expression of the markers CD2, CD4, CD8 and CD 19. After mitogenic proliferation two populations appeared, one corresponding to non-stimulated cells, and the other consisting of larger cells which showed relatively high expression of adenosine deaminase on their surface. The increase was similar to that observed for CD71 expression, and paralleled the increase in 3H-thymidine incorporation. There was a correlation between ADA and CD71 expression (r = 0-92 for phytohaemagglutinin (PHA) and 0 97 for pokeweed mitogen (PWM)). These results suggest a role for ecto-adenosine deaminase in lymphocyte proliferation and/or triggering.

SUMMARY A group of 54 patients with primary retinitis pigmentosa were studied and the following findings are described: response of lymphocytes to stimulation by phytohaemagglutinin (PHA); response of lymphocytes to stimulation by xenogenic retinal extract; distribution of T and T-active lymphoid populations; total suppressor activity induced by concanavalin-A (con-A). The results obtained showed a reduction in the response to PHA (p<005), a positive response of 26/45 (p

Summary The authors studied the T‐ and B‐lymphocyte sub‐populations, the stimulation of the lymphocytes with phytohaemagglutinin and pokeweed mitogen, the non‐specific T suppressor activity and the amounts of serum IgE in a group of thirty‐four patients with atopic dermatitis. Comparison with a group of 100 healthy controls revealed a diminution in the T sub‐population, an increase in the B sub‐population, no change in the response index to stimulation with phytohaemagglutinin or pokeweed mitogen, a diminished T‐suppressor activity and an increase in the level of serum IgE.

The expression of surface adenosine deaminase (ADA) and CD26 in activated human T cells was studied by flow cytometry. PBLs and CD3+ or CD4+ cells, when subjected to a variety of stimuli (anti-CD3 Abs plus IL-2 or phorbol esters), presented two structurally different cell populations, which differed in size and cellular complexity (populations B1 and B2). In PBLs triggered by an anti-CD3 mAb there was no significant increase of expression of either surface ADA or CD26 in cells of population B1, whose structure is similar to that of nonstimulated cells. In contrast, there was a significant increase in the percentage of expression of ADA and CD26 in the population B2, which corresponds to structurally more complex and larger cells. In the case of activation via TCR-CD3 but in the presence of IL-2 or via phorbol esters, the increase was found in cells from both populations, but B2 cells always showed a higher percentage of expression than B1 cells. The results of increased expression of surface ADA and CD26 were similar in whole T cells or in purer preparations such as CD3+ or CD4+ lymphocytes. Polyclonal Abs against ADA were not able to induce an activation response in T cells even when cross-linked by a secondary Ab. Interestingly, these Abs produced anergy in CD4+ cells subjected to an anti-CD3 stimulus. In contrast, addition of ADA produced an enzyme-independent synergism in the response through the TCR-CD3 complex. In T cells, ADA and CD26 colocalized on the surface of T cells; thus, the effect of exogenous ADA seems to be mediated by CD26 molecules that are not interacting with endogenous ADA (spare CD26 molecules). The presence of spare CD26 molecules on the surface of CD4+ cells was demonstrated by flow cytometry in the presence of exogenous ADA and also by confocal microscopy. The set of results strongly indicates that ADA binding to CD26 produces a costimulatory response in T cell activation events.