Phenotypic abnormalities of splenic and bone marrow B cells in lpr and gld mice

E. A REAP; M. L PIECYK; Alyce Oliver; E. S SOBEL; T WALDSCHMIDT; P. L COHEN; R. A EISENBERG

doi:10.1006/clin.1996.0004

Back

Phenotypic abnormalities of splenic and bone marrow B cells in lpr and gld mice

Journal article

Open access

Phenotypic abnormalities of splenic and bone marrow B cells in lpr and gld mice

E. A REAP, M. L PIECYK, Alyce Oliver, E. S SOBEL, T WALDSCHMIDT, P. L COHEN and R. A EISENBERG

Clinical immunology and immunopathology, Vol.78(1), pp.21-29

1996

DOI: 10.1006/clin.1996.0004

PMID: 8599880

Files and links (1)

url

https://doi.org/10.1006/clin.1996.0004View

Published (Version of record) Open Access

Abstract

Mice homozygous for the mutantFasgenelprdevelop generalized lymphoproliferation and produce autoantibodies resembling those found in human SLE. We have previously shown that these autoantibodies are produced by B2 cells rather than B1 cells and that the autoantibody-producing B cells are intrinsically abnormal. We investigated further thelprB cell with a large panel of antibodies to B-cell surface markers to identify phenotypic abnormalities. B cells from spleen and bone marrow of age-matched congenic mice differing only at thelprlocus were examined by flow cytometry. Two consistent phenotypic differences were identified. First, spleen cells from olderlprmice had an increase in the number and percentage of IgM+B cells expressing low levels of CD23. Second,lprbone marrow had decreased numbers of B220h1IgM+-syndecan-1+CD23+B cells. All other markers tested, except the previously identified modest increase of Ia onlprspleen cells, showed no consistent differences. B cells fromgldmice showed the same phenotypic abnormalities as those fromlpr.Compared to T cells, the relative paucity of cell surface marker differences betweenlprand +/+ B cells suggests that B cells may have fewer regulatory mechanisms to silence autoreactive specificities. The phenotypic differences identified may provide clues to the mechanism of autoantibody production inlprmice, while the overwhelming phenotypic similarity betweenlprand +/+ B cells suggests that the major abnormality oflprB cells may lie in their specificity, that is, in their inability to delete autoreactive subsets.

Immunopathology

Experimental and animal immunopathology. Animal models

Biological and medical sciences

Medical sciences

Details

Title: Subtitle: Phenotypic abnormalities of splenic and bone marrow B cells in lpr and gld mice
Creators: E. A REAP - Departments of Medicine and Microbiology/Immunology, University of North Carolina, Chapel Hill, North Carolina 27599-7280, United States
M. L PIECYK - Departments of Medicine and Microbiology/Immunology, University of North Carolina, Chapel Hill, North Carolina 27599-7280, United States
Alyce Oliver - Departments of Medicine and Microbiology/Immunology, University of North Carolina, Chapel Hill, North Carolina 27599-7280, United States
E. S SOBEL - Departments of Medicine and Microbiology/Immunology, University of North Carolina, Chapel Hill, North Carolina 27599-7280, United States
T WALDSCHMIDT - Departments of Medicine and Microbiology/Immunology, University of North Carolina, Chapel Hill, North Carolina 27599-7280, United States
P. L COHEN - Departments of Medicine and Microbiology/Immunology, University of North Carolina, Chapel Hill, North Carolina 27599-7280, United States
R. A EISENBERG - Departments of Medicine and Microbiology/Immunology, University of North Carolina, Chapel Hill, North Carolina 27599-7280, United States
Resource Type: Journal article
Publication Details: Clinical immunology and immunopathology, Vol.78(1), pp.21-29
DOI: 10.1006/clin.1996.0004
PMID: 8599880
NLM abbreviation: Clin Immunol Immunopathol
ISSN: 0090-1229
eISSN: 1090-2341
Publisher: Academic Press; San Diego, CA; New York, NY; Boston
Language: English
Date published: 1996
Academic Unit: Pathology
Record Identifier: 9984047878302771

Metrics

12 Record Views

24 Times Cited - Web of Science