Proliferation of cytotoxic T‐cells, a prerequisite for the development of antitumor vaccines, was induced by 1, but not by its partial structures A and B. The conjugate 1 containing a tumor‐associated Sialyl–TN–MUC‐1 glycopeptide antigen A and a T‐cell epitope B of tetanus toxin was synthesized by fragment condensation on a solid phase.

The disialoganglioside GD3 (CD60 a) and its O-acetylated variants have previously been described as surface molecules of human T lymphocytes of the peripheral blood system. Here we report the expression of the 9-O-, and 7-O-acetylated disialoglycans of GD3 (CD60 b and CD60 c respectively) on human tonsillar lymphocytes. CD60 b and c are surface-expressed on activated germinal centre B cells and colocalize in raft-like structures on the cell surface together with the cytoplasmic tyrosine kinase Lyn and Syk. Addition of CD60 b and c mAb together with anti-IgM/IL-4 to in vitro cultivated tonsillar B cells resulted in a costimulatory effect. During spontaneous and staurosporine-induced apoptosis a distinct population of activated annexin V+/CD60 b+/CD60 c- B cells was observed. CD60 b and c are also found on cells of the extrafollicular T cell area. On tonsillar T cells, CD60 b mAb had a costimulatory effect together with PHA while CD60 c mAb alone was sufficient to induce proliferation. In further contrast to B cells, during apoptosis a distinct CD60 b+ T cell subpopulation was not observed. Together, surface-expressed CD60 b and c are differently expressed on tonsillar B and T cells and may be involved in the regulation of activation and apoptosis of lymphocytes in secondary lymphatic tissue.

Die Proliferation cytotoxischer T‐Zellen, eine Voraussetzung für die Entwicklung von Antitumor‐Impfstoffen, wird von 1, aber nicht von den Teilstrukturen A und B induziert. Durch Fragmentkondensation an fester Phase wird das Konjugat 1 aus einem tumorassoziierten Sialyl‐TN‐MUC‐1‐Glycopeptid‐Antigen A und einem Tetanustoxin‐T‐Zellepitop B aufgebaut.

Properdin is the only known positive regulator of the alternative pathway of complement activation. Northern blot analysis of cell lines derived from fibroblasts, B-cells, hepatoma cells, and cells of the monocyte-macrophage lineage revealed properdin expression only in the myelomonocytic cell line HL-60, in the monoblastic cell line U-937 and in the monocytic line Mono Mac 6. Culture of Mono Mac 6 cells for 24 h with phorbol 12-myristate 13-acetate, bacterial lipopolysaccharide and the cytokines interleukin-lb and tumour necrosis factor-a enhanced mRNA abundance, with the strongest effect (tenfold) being observed with the lipopolysaccharide. In contrast, recombinant interferon-y consistently halved properdin mRNA abundance. The same pattern was found for the secretion of properdin as detected by ELISA of Mono Mac 6 supernatants. The suppressive effect of interferon-y on properdin mRNA abundance was also demonstrated for primary blood monocytes. The data suggest that the expression and secretion of this complement regulatory protein by monocytes is differentially regulated by cytokines and link the immune response with alternative pathway activation.Properdin is one of the six plasma glycoproteins which constitute the alternative pathway of complement activation [I, 21. Three of these proteins (C3 and factors B and D) form the activation system, whereas the other three (properdin and factors H and I) are regulatory components. Properdin is essential for optimal rates of complement activation by virtue of its ability to bind and stabilize the inherently labile C3 and C5 convertase complexes (C3bBb and C3b,Bb) of the alternative pathway. Stabilization of these complexes by properdin accelerates activation, promotes C3b attachment, and enhances C5 cleavage leading to increased cytolysis and phagocytosis. The importance of this positive regulatory complement component is illustrated by the symptoms experienced by properdin-deficient individuals [3, 41. Approximately 50% of the patients suffer from severe, fulminant, pyrogenic bacterial infections, usually meningococcal with a fatality rate approaching 75%. The deficiency is transmitted as an X-linked, recessive trait consistent with studles mapping the gene to Xp11.23-Xp11.3 [5, 61. In plasma, properdin is present (5-15 pg/rnl) as a polydisperse mixture of cyclic polymers, mainly dimers, trimers, and tetramers, in the ratio 20 : 54:26, formed by the (presumably head-to-tail) interac- Abbreviations. FCS, foetal-calf serum heat-inactivated for 2 h at 56°C; IFN-y, recombinant interferon-y ; IL-1, interleukin-lp; LPS, bacterial lipopolysaccharide; Me,SO, dimethylsulfoxide; NaCW,, 137 mM NaC1,2.6 mM KCl, 4 mM Na2HP04, and 1.8 mM KH,PO, adjusted to pH 7.4; PMA, phorbol 12-myristate 13-acetate; TNF-a, tumour necrosis factor-a.Leicester Royal Infirmary, Leicester LE 1 5WW, England tions of a single, asymmetric monomer of approximately 46kDa [7, 81. cDNA cloning and sequencing provided the complete primary structure of human properdin [9] which is very similar (76% identity)...

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