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[Cancer Research 48, 37-40, January 1, 1988]
© 1988 American Association for Cancer Research

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Molecular Pathways of Adhesion in Spontaneous Rosetting of T-Lymphocytes to the Hodgkin's Cell Line L428

Martin E. Sanders1, M. William Makgoba, Eileen H. Sussman, Gale E. G. Luce, Jeffrey Cossman and Stephen Shaw

The Immunology Branch and the Laboratory of Pathology, National Cancer Institute, NIH, Bethesda, Maryland 20892

Spontaneous rosetting of T-lymphocytes to Reed-Sternberg cells has been observed both in vitro and in vivo but its molecular mechanism has not been defined. We have investigated such rosetting using the Hodgkin's cell line L428. L428 expresses high levels of LFA-3 and ICAM-1, both of which are ligands for T-cell adhesion. Monoclonal antibody inhibition of spontaneous rosetting indicated that it is not dependent on the T-cell receptor complex but is largely mediated by interaction of T-cell CD2 (T11/E-rosette receptor) with its ligand LFA-3 on L428 cells. Studies using an alternate assay of adhesion (conjugate formation) confirm the roles of CD2/LFA-3 and also implicate a second mode of binding via LFA-1 on T-cells to ICAM-1 on L428. These data explain the previously reported finding of T-cell rosetting with Reed-Sternberg cells as an exaggeration of normal antigen-independent T-cell adhesion.

1 To whom requests for reprints should be addressed, at NIH, Bldg. 10, Room 4B17, Bethesda, MD 20892.

Received 6/25/87. Revised 9/23/87. Accepted 9/28/87.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1988 by the American Association for Cancer Research.