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

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Lamon, E. W. Articles by Ghanta, V. Search for Related Content PubMed Articles by Lamon, E. W. Articles by Ghanta, V.

IgM Complex Receptors on Subpopulations of Murine Lymphocytes¹

From the Veterans Administration Hospital, Departments of Surgery and Microbiology, University of Alabama in Birmingham School of Medicine, Birmingham, Alabama 35294, and the Department of Tumor Biology, Karolinska Institute, Stockholm, Sweden

Abstract

Murine lymphocytes from spleen, lymph node, and thymus were examined for IgM complex receptors. Lymphocytes from all three organs were found to bind SRBC sensitized with IgM from various sources including: primary anti-SRBC serum, murine and rabbit anti-Escherichia coli LPS sera, and a murine IgM myeloma (MOPC 104E). Rosette formation by lymphocytes with IgM-sensitized SRBC was inhibited by soluble antigen-IgM complexes but not by IgM or antigen alone. Rosette formation was also inhibited by human IgM (Fc)_5µ but not by Fab µ. Antiserum and complement treatment of the cells and subsequent recovery of the viable cells by trypsinization, filtration, and washing revealed the IgM rosette-forming cell (RFC) in the thymus to be a T cell. Spleen on the other hand was found to contain both B and T cells capable of binding IgM sensitized SRBC. Removal of both B and T cells from spleen cell suspensions eliminated all IgM RFC. The IgM complex receptor was found to be trypsin insensitive. Anti-Ig column fractionation enriched IgM RFC in spleen and lymph node suspensions passed through the columns, whereas cells bearing surface Ig, IgG complex receptors, and C3 receptors were retained in the columns.

Footnotes

¹ This work was performed persuant to Contracts N01-CP-43394 within the division of Cancer Cause and Prevention, The Virus Cancer Program, N01-CB-33866, within the Division of Cancer Biology and Diagnosis, and Grant CA A1 1723-01 National Cancer Institute, National Institutes of Health. Credit is given to the Birmingham Veterans Administration Hospital Project No. 5132-01. Grants were also received from the Swedish Cancer Society.

² Recipient of a Research Career Development Award from the National Cancer Institute.

³ Recipient of United States Public Health Service Training Grant HL-05677-09 from the Department of Medicine, Section of Immunology, University of California, San Francisco, California. Present address: Old Dominion University, Department of Microbiology, Norfolk, Virginia 23508.