To elucidate the pathogenesis of hematogenous Candida infections, we developed an in vitro model of Candida adherence to and penetration of human endothelial cells. We enhanced or inhibited adherence in order to probe mechanisms of attachment. Adherence of Candida albicans showed a linear relation to Candida inoculum (range, 10(2)-10(5) cfu, r = .99, P less than .01) and exceeded that of less virulent Candida species and that of Saccharomyces cerevisiae (P less than .01). Candida immune serum blocked attachment (greater than 95% inhibition; P less than .001), however, this activity was abolished by immunoprecipitation of immune serum with C. albicans mannan (P less than .001) and was unaffected by immunoprecipitation with S. cerevisiae mannan or by adsorption with particulate chitin. Adherence was diminished by exposing C. albicans to heat (greater than 99% inhibition; P less than .01), UV light (98% inhibition; P less than .01), or sodium periodate (greater than 72% inhibition; P less than .01). An extract from heat-exposed C. albicans blocked adherence (greater than 51% inhibition; P less than .001). Transmission electron microscopy demonstrated that viable or killed Candida organisms were attached to endothelial cells, were enveloped by membrane processes from the endothelial cell surface, and were incorporated into the endothelial cells within phagosomes. Cytochalasin B blocked incorporation without blocking surface attachment.

Normal human T cells proliferate vigorously when stimulated with autologous non-T cells. This autologous mixed lymphocyte reaction (MLR) between T and non-T cells was defective in patients with active systemic lupus erythematosus (SLE) In contrast, T cells and non-T cells from active SLE patients behaved normally as responding and stimulating cells, respectively, in the allogeneic MLR. Systemic lupus erythematosus (SLE) is a complex multisystem autoimmune disease. One of its most prominent features is the presence of a wide variety of autoantibodies in the serum. In addition, several T cell defects have been described in patients with active SLE. It has been postulated that the excessive production of autoantibodies is due to some abnormality in B cell regulation by T cells (1, 2). More specifically, evidence has been presented to suggest a relative lack of suppressor T cell function in such patients (3-5).In the course of our studies of suppressor T cell function in patients with SLE (5), we made the unexpected observation that, when lymphocytes from patients with SLE were used, the autologous mixed lymphocyte reaction (MLR) failed to occur.That is, whereas T cells from normal individuals proliferate vigorously in response to autologous non-T cells, T cells from SLE patients failed to proliferate normally in response to autologous non-T cells. In these studies we have investigated the reason for this defect in patients with SLE.Because it has been recently proposed that "autologous MLR reflect a mechanism by which T lymphocytes regulate lymphocyte function" (6), the absence of such a reaction in the lymphocytes of patients with SLE is particularly provoca-

Erythrocytes infected with the late stages of the human malarial parasite Plasmodium falciparum became attached to a subpopulation of cultured human endothelial cells by knoblike protrusions on the surface of the infected erythrocytes. Infected erythrocytes did not bind to cultured fibroblasts; uninfected erythrocytes did not bind to either endothelial cells or fibroblasts. The results suggest a specific receptor-ligand interaction between endothelial cells and a component, components, in the knobs of the infected erythrocytes.

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