Premium
Interleukin 2 is a proliferative signal for B cells from autoimmune mice
Author(s) -
Lehmann Kathrin R.,
Kotzin Brian L.,
Portanova Joseph P.,
Santoro Thomas J.
Publication year - 1986
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.1830160913
Subject(s) - biology , immunology , microbiology and biotechnology
Abstract T cells from murine lupus strains manifest complex defects in interleukin 2 (IL 2) production and receptor expression. The capacity of B cells from such mice to utilize IL2 as a growth factor has not been previously reported and is examined herein. Anti‐Thy‐1.2 plus complement‐treated spleen cells from 6–8‐week‐old autoimmune MRL‐ Ipr/lpr mice and from age and sex‐matched immunologically normal CBA/J mice were cultured with lipopolysaccharide (LPS) for 36 h and analyzed for the expression of IL 2 receptors using the monoclonal antibody 7D4. The percentage of B cells expressing IL2 receptors was comparable in MRL‐ lpr/lpr and CBA/J mice. In contrast to those from CBA/J, BALB/c and (BALB/c × NZW)F 1 mice, LPS‐stimulated B cells from MRL ‐lpr/lpr and from (NZB × NZW)F 1 mice were capable of proliferating in response to IL 2. Fractionation of MKL ‐lprl/lpr B cells using Percoll gradient density separation demonstrated that the IL2‐responsive population consisted predominantly of large cells. In addition, unfractionated B cells from MRL ‐lpr/lpr mice were found to be substantially more responsive to IL2 than those from CBA/J and BALB/c mice following activation with anti‐immunoglobulin plus LPS. The hyper‐responsiveness to IL 2 may be a consequence of the state of activation of autoimmune B cells and is of potential importance in the pathogenesis of systemic lupus erythematosus.