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 Baker, P. J. Articles by Prescott, B. Search for Related Content PubMed Articles by Baker, P. J. Articles by Prescott, B.

Regulation of the Antibody Response to Type III Pneumococcal Polysaccharide

II. Mode of Action of Thymic-Derived Suppressor Cells

From the Laboratory of Microbial Immunity, and the Laboratory of Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014

Abstract

The present study was conducted primarily to obtain information concerning the mechanism by which suppressor thymic-derived (T) cells influence the magnitude of the antibody response to type III pneumococcal polysaccharide (SSS-III). This was accomplished by examining the effects of treatment with antilymphocyte serum (ALS) and Velban, a mitotic inhibitor, on the kinetics for the appearance of plaque-forming cells (PFC) in mice immunized with SSS-III. Without ALS-treatment, the kinetics were essentially biphasic. First, there was a phase during which PFC appeared at a relatively rapid rate; this was followed by a phase during which the rate of appearance of PFC gradually declined until maximal numbers were attained. In contrast, similar rate changes were not noted for mice given ALS; here, PFC increased at a uniform exponential rate throughout the 1st 5 days of the antibody response. Velban completely arrested the development of additional PFC in ALS-treated but not non-ALS-treated mice. These findings indicate that suppressor T cells act primarily by limiting the extent to which antibody-forming bone marrow-derived cells proliferate following immunization.

Footnotes

¹ Correspondence and reprint requests should be addressed to Phillip J. Baker, Laboratory of Microbial Immunity, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20014.