Independent ligand occupancy and cross-linking of surface Ig and Fcγ receptors downregulates B-lymphocyte function. evaluation in various B-lymphocyte populations

F. Uher, Howard B. Dickler

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

When two distinct B-lymphocyte membrane receptors (Fcγ R and slg) are independently occupied by their respective multivalent ligands, inhibition of the antibody-forming cell response occurs but proliferation is not inhibited. This regulatory signal was examined in various B-lymphocyte populations. Unprimed B lymphocytes from immune deficient CBA/N and autoimmune MRL/1 mice were responsive to this regulatory signal. In contrast, unprimed B lymphocytes from autoimmune NZB mice and antigen-primed B lymphocytes from normal DBA/2 mice were not. Together with previous results, these data suggest that resting B lymphocytes which have not encountered antigen are most susceptible to this regulatory signal. Lack of responsiveness to this downregulatory signal may contribute to the hyper-responsiveness of NZB B lymphocytes.

Original languageEnglish
Pages (from-to)1177-1181
Number of pages5
JournalMolecular Immunology
Volume23
Issue number11
DOIs
Publication statusPublished - 1986

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Fc Receptors
B-Lymphocytes
Down-Regulation
Ligands
Population
Inbred NZB Mouse
Antigens
Inbred DBA Mouse
Membranes
Antibodies

ASJC Scopus subject areas

  • Molecular Biology
  • Immunology

Cite this

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AB - When two distinct B-lymphocyte membrane receptors (Fcγ R and slg) are independently occupied by their respective multivalent ligands, inhibition of the antibody-forming cell response occurs but proliferation is not inhibited. This regulatory signal was examined in various B-lymphocyte populations. Unprimed B lymphocytes from immune deficient CBA/N and autoimmune MRL/1 mice were responsive to this regulatory signal. In contrast, unprimed B lymphocytes from autoimmune NZB mice and antigen-primed B lymphocytes from normal DBA/2 mice were not. Together with previous results, these data suggest that resting B lymphocytes which have not encountered antigen are most susceptible to this regulatory signal. Lack of responsiveness to this downregulatory signal may contribute to the hyper-responsiveness of NZB B lymphocytes.

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