Helmholtz Gemeinschaft


T helper cell membranes promote IL-4-independent expression of germ-line Cγ1 transcripts in B cells

Item Type:Article
Title:T helper cell membranes promote IL-4-independent expression of germ-line Cγ1 transcripts in B cells
Creators Name:Schultz, C.L., Rothman, P., Kühn, R., Kehry, M., Müller, W., Rajewsky, K., Alt, F. and Coffman, R.L.
Abstract:Studies using plasma membranes from activated Th cell clones (Th membranes) to stimulate B cells have shown that both a contact-mediated activation signal plus Th-derived cytokines are required for antibody production. In order to clearly separate and define the role of these two signals in isotype switching, B cells were stimulated with Th membranes in the presence or absence of cytokines, and the transcriptional activity of the unrearranged H chain loci was determined. In the presence of Th membranes, two known switch factors were shown to specifically induce germ-line transcription of the same H chain loci as in LPS-stimulated B cells (IL-4 induced C gamma 1 and C epsilon transcription, transforming growth factor-beta induced C alpha transcription). The contact-mediated activation signal provided by the Th membranes, in the absence of any added cytokines, resulted in the specific induction of C gamma 1 germ-line transcription, and thus functioned as a switch signal for IgG1. These findings provide a mechanism for previously observed IL-4-independent isotype switching to IgG1.
Keywords:B-Lymphocytes, Cell Communication, Cell Membrane, Gene Expression Regulation, Genetic Transcription, Helper-Inducer T-Lymphocytes, Immunoglobulin Constant Regions, Immunoglobulin G, Immunoglobulin {gamma}-Chains, Immunoglobulin Genes, Interleukin-4, Lymphocyte Activation, Messenger RNA, Animals, Inbred BALB C Mice, Mice
Source:Journal of Immunology
Publisher:American Association of Immunologists
Page Range:60-64
Date:1 July 1992
Official Publication:https://doi.org/10.4049/jimmunol.149.1.60
PubMed:View item in PubMed

Repository Staff Only: item control page

Open Access
MDC Library