HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Data Supplement Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Deola, S. Articles by Marincola, F. M. PubMed PubMed Citation Articles by Deola, S. Articles by Marincola, F. M.

Helper B Cells Promote Cytotoxic T Cell Survival and Proliferation Independently of Antigen Presentation through CD27/CD70 Interactions¹

Sara Deola^*, Monica C. Panelli^*, Dragan Maric, Silvia Selleri^*,¶, Natalia I. Dmitrieva, Ching Y. Voss, Harvey Klein^*, David Stroncek^*, Ena Wang^* and Francesco M. Marincola^2,*

^* Infectious Disease and Immunogenetics Section, Department of Transfusion Medicine and Department of Laboratory Medicine, Clinical Center, Flow Cytometry Facility, National Institute of Neurological Disorders and Stroke, and Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892; and ^¶ Department of Human Morphology, Universitá degli Studi di Milano, Milan, Italy

CD8-expressing cytotoxic T cell (CTL) interactions with APCs and helper T cells determine their function and ability to survive. In this study, we describe a novel interaction independent of Ag presentation between activated CTLs and bystander CD19-expressing B lymphocytes. Ag-stimulated CTLs serially engage autologous B lymphocytes through CD27/CD70 contact that promotes their survival and proliferation. Moreover, these interactions induce the release of proinflammatory cytokines that follows two general patterns: 1) an epitope-dependent enhancement of cytokine release, and 2) a previously undiscovered coordinate release of cytokines independent of epitope exposure. The latter includes chemoattractants targeting activated T cells. As a result, activated T cells are attracted to B cells, which exert a "helper" role in lymphatic organs or in areas of inflammation. This observation provides a mechanistic explanation to previously reported experimental observations suggesting that B cells are required for T cell priming in vivo.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported in part by Fondazione Italiana per la Ricerca sul Cancro.

² Address correspondence and reprint requests to Dr. Francesco Marincola, Infectious Disease and Immunogenetics Section, Department of Transfusion Medicine, Clinical Center, National Institutes of Health, Building 10, Room 1N224, 9000 Rockville Pike, Bethesda, MD 20892. E-mail address: fmarincola{at}mail.nih.gov

³ Abbreviations used in this paper: IVS, in vitro sensitization; TIL, tumor-infiltrating lymphocyte; T_CM, central memory T cells; T_EM, effector memory T cells.