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We found that human peripheral B and T cells differed in the surface expression of α2-6 sialylated type 2 chain glycans. In contrast to B cells, T cells expressed only sialoglycans with repeated N-acetyllactosamine (Galß1-4GlcNAc) disaccharides. This finding was based on the specificity of the monoclonal antibodies HB6, HB9 (CD24), HD66 (CDw76), FB21, and CRIS4 (CDw76) with the α2-6 sialylated model gangliosides IV⁶NeuAcnLc₄Cer (2-6 SPG), VI⁶NeuAcnLc₆Cer (2-6 SnHC), VIII⁶NeuAcnLc₈Cer (2-6 SnOC), and X⁶NeuAcnLc₁₀Cer (2-6 SnDC). We found that, in addition to their common requirement of an α2-6 bound terminal sialic acid for binding, the antibodies displayed preferences for the length of the carbohydrate backbones. Some of them bound mainly to 2-6 SPG with one N-acetyllactosamine (LacNAc) unit (HB9, HD66); others preferentially to 2-6 SnHC and 2-6 SnOC, with two and three LacNAc units, respectively (HB6 and FB21); and one of them exclusively to very polar α2-6 sialylated type 2 chain antigens (CRIS4) such as to 2-6 SnOC and even more polar gangliosides with three and more LacNAc units. These specificities could be correlated with the cellular binding of the antibodies as follows: whereas all antibodies bound to human CD 19 positive peripheral B cells, their reactivity with CD3 positive T cells was either nearly lacking (HD66, HB9), intermediate (about 65%: HB6, FB21) or strongly positive (CRIS4, 95%). Thus, the binding of the antibodies to 2-6 sialylated glycans with multiple lactosamine units appeared to determine their binding to T-cells.

Background: Monoclonal CD4 antibodies are among the most potent immunomodulatory agents in various experimental models of autoimmune disease, including murine lupus erythematosus. Objective: The aim of this study was to evaluate the toxicity and therapeutic efficacy of achimeric monoclonal CD4 antibody, cM-T412, in patients with cutaneous lupus erythematosus (LE). Methods: Five patients with severe cutaneous LE lesions received intravenously a total of275, 400, or 475 mg of cM-T412 in single doses of 20 to 50 mg during a period of 5 to 8 weeks. Results: CD4 antibody treatment induced a long-lasting decrease in disease activity. Itresulted in healing of LE skin lesions, a reconstituted responsiveness to conventional treatment, or both. Despite a substantial depletion of circulating CD4^+ T lymphocytes, no clinical signs of immunosuppression were noted. Conclusion: Monoclonal CD4 antibodies should be considered as a novel treatment for themanagement of severe cutaneous LE.

Background: The cellular basis for the mechanism of specific hyposensitization is still unclear. Objective: We prospectively studied the effect of immunotherapy on allergen-induced proliferation and Fc@eR2/CD23 expression of lymphocytes. Methods: Mononuclear cells prepared from the peripheral blood of 22 patients with grass pollen (GP) allergy before, during, and after a preseasonal immunotherapy period with GP were stimulated with GP or control antigens. Tritiated thymidine uptake and percentage of CD23^+B cells were determined daily during days 6 to 8 and compared with lymphocyte responsiveness of 11 only symptomatically treated atopic patients and 14 nonatopic individuals. Results: GP-induced lymphocyte proliferative response of both hyposensitized and symptomatically treated GP-allergic patients decreased markedly before the pollen season and rose again after seasonal allergen exposure, whereas a long-lived decrease in GP-induced Fc@eR2/CD23^+ B cells was only observed in GP-treated patients. Alterations in Fc@eR2/CD23 expression were closely related to changes in symptoms and medication requirement during the following pollen season. In contrast, immunotherapy had no effect on Fc@eR2/CD23 expression of B cells without stimulation or on B cells cultured in the presence of control antigens. Conclusion: Because Fc@eR2/CD23 expression on B cells is antagonistically regulated by the cytokines interleukin-4 and interferon-@c, the decrease of allergen-induced Fc@eR2/CD23^+ B cells indicates an altered cytokine secretion pattern of the allergen-specific T lymphocytes with a predominance of interferon-@c. (J ALLERGY CLIN IMMUNOL 1995;95:77-87.)