gld and lpr hematopoietic cell transfers: common and different serological features of the C57BL/6 chimeras.

Abstract:

:Homozygosity for either the lpr (lymphoproliferation) or the gld (generalized lymphoproliferative disease) mutation in mice causes the development of strikingly similar hyperglobulinemia and lymphoproliferative syndromes. Nevertheless, previous studies of various C57BL/6 chimeras obtained by reconstitution of irradiated recipients with hematopoietic cells (HC), differing at the bg, gld, lpr, and/or nu loci, showed that the lpr and gld syndromes had distinct etiologies. The [lpr-->lpr], [gld-->gld], and [gld-->wild] chimeras developed lymphoid hyperplasia, while the [lpr-->wild, bg, or gld] and [nulpr-->wild or bg] chimeras developed a severe persistent lymphoid aplasia. We now show that the serological status (immunoglobulin (Ig) levels and Ig isotype distribution) of the [lpr-->lpr], [gld-->gld], and [gld-->wild] chimeras were roughly equivalent to those of genetic lpr and gld mice. Despite their lymphoid aplasia, all the [lpr-->non-lpr] chimeras displayed surprisingly normal serum Ig levels, similar to [wild-->wild] control chimeras, although always with some abnormal isotype profile. In fact, an early but transient increase of serum IgG1 levels was found in all [lpr-->wild, bg, or gld], [lpr-->lpr], [nulpr-->wild or bg], [wild-->lpr], and [gld-->wild or gld] types of chimeras. Despite a common early behavior, the host type and/or the gld or lpr HC origin may cause later divergences of the gld or lpr HC grafted chimeras.

journal_name

Cell Immunol

journal_title

Cellular immunology

authors

Velin D,Goettelfinger P,Froidevaux S,Loor F

doi

10.1006/cimm.1993.1116

subject

Has Abstract

pub_date

1993-05-01 00:00:00

pages

331-45

issue

2

eissn

0008-8749

issn

1090-2163

pii

S0008-8749(83)71116-0

journal_volume

148

pub_type

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