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 Immunoljournal_title
Cellular immunologyauthors
Velin D,Goettelfinger P,Froidevaux S,Loor Fdoi
10.1006/cimm.1993.1116subject
Has Abstractpub_date
1993-05-01 00:00:00pages
331-45issue
2eissn
0008-8749issn
1090-2163pii
S0008-8749(83)71116-0journal_volume
148pub_type
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journal_title:Cellular immunology
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journal_title:Cellular immunology
pub_type: 杂志文章
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journal_title:Cellular immunology
pub_type: 杂志文章
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journal_title:Cellular immunology
pub_type: 杂志文章
doi:10.1006/cimm.1997.1238
更新日期:1998-01-10 00:00:00
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journal_title:Cellular immunology
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journal_title:Cellular immunology
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journal_title:Cellular immunology
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journal_title:Cellular immunology
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journal_title:Cellular immunology
pub_type: 杂志文章
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更新日期:1995-01-01 00:00:00
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journal_title:Cellular immunology
pub_type: 杂志文章,评审
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journal_title:Cellular immunology
pub_type: 杂志文章
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更新日期:1987-09-01 00:00:00
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journal_title:Cellular immunology
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abstract::Interleukins play a role in the process of T-cell development and, like other cytokines, seem able to modulate apoptosis. Interleukin-2 has been reported to inhibit apoptotic cell death of thymocytes induced in vitro by either activation of CD3/TCR complex or treatment with glucocorticoid hormone. We demonstrate here ...
journal_title:Cellular immunology
pub_type: 杂志文章
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更新日期:1993-01-01 00:00:00