T cell abnormalities in NZB mice occur independently of autoantibody production.

Taurog, Joel D.; Raveché, Elizabeth; Smathers, P A; Glimcher, L H; Huston, David P.; Hansen, Carl T.; Steinberg, Alfred D.

doi:10.1084/jem.153.2.221

Cited by 71 publications

(17 citation statements)

References 45 publications

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“…These results force a reeval- INTRODUCTION The effect of the X chromosome-linked recessive immune deficiency gene, xid,' upon the immune system has been under intensive study for the past 10 yr with regard to both basic immunology (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13) (14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25). It (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13).…”

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confidence: 99%

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Ability of the xid gene to prevent autoimmunity in (NZB X NZW)F1 mice during the course of their natural history, after polyclonal stimulation, or following immunization with DNA.

Steinberg¹,

Smathers²,

Frederiksen³

et al. 1982

J. Clin. Invest.

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123

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A B S T R A C T F, hybrid offspring of New ZealandBlack mothers and New Zealand White fathers [(NZB X NZW)F1] female mice develop antibodies to singlestranded (ss) and native DNA, immune complex glomerulonephritis, massive proteinuria, and premature death with renal failure. By a series of matings, congenic (NZB X NZW)Fj * xid/xid mice were prepared. These mice were different from (NZB X NZW)Fj mice in having the X chromosome-linked immune deficiency gene, xid, in homozygous form. Such congenic (NZB X NZW)F, xid/xid females failed to develop antibodies to single-stranded or native DNA. They also failed to develop fatal renal disease as measured by proteinuria, glomerular histology, glomerular immunofluorescence, and survival.To control for unknown genetic factors, studies were performed with littermates that were derived by mating NZB * xid/+ females with NZW * xid/Y males such that the resulting offspring were either (NZB X NZW)F1. xid/xid (and therefore "defective") or (NZB X NZW)F1 . xid/+ [phenotypically like (NZB X NZW)Fl]. In these and in additional studies, mice were housed in the same cages and identified by ear tagging so as to avoid possible environmental variations from cage to cage. In these studies, xid/xid mice failed to develop the characteristic signs of autoimmunity, whereas the controls did. Similar results were also obtained with (NZW X NZB)F1 xid/xid mice compared with (NZW X NZB)Fj xid/+ mice.The effect of xid/xid upon (NZB X NZW)F1 mice was further investigated by assessing responses to immunization and polyclonal B cell activation in vivo.

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confidence: 99%

“…The presence of xid in homozygous or hemizygous form causes a marked reduction in all signs of autoimmunity in NZB mice (17)(18)(19)(20)(21)(23)(24)(25). However, this disease prevention is overcome by immunization or polyclonal immune stimulation (16,19,(23)(24)(25).…”

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confidence: 99%

Ability of the xid gene to prevent autoimmunity in (NZB X NZW)F1 mice during the course of their natural history, after polyclonal stimulation, or following immunization with DNA.

Steinberg¹,

Smathers²,

Frederiksen³

et al. 1982

J. Clin. Invest.

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123

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“…When bred onto autoimmune strains, xid dramatically retards the development of their B cell hyperactivity and autoantibody production (22,23). Nevertheless, xid did not significantly alter expression of 8.4-kb MCF transcripts in NZB and BXSB mice ( Figure 6).…”

Section: Effects Of Yuumentioning

confidence: 98%

Expression of an endogenous retroviral transcript is associated with murine lupus

Krieg¹,

Khan²,

Steinberg³

1989

Arthritis & Rheumatism

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We have been investigating whether murine lupus is associated with endogenous type C retroviral expression. We used Northern blot analyses and oligonucleotide probes, which are able to distinguish the envelope genes of the xenotropic and mink cell focusforming (MCF) classes of type C retroviruses. Xenotropic expression in the spleen varied markedly among inbred mouse strains; although all strains expressed a 1.8‐kb transcript, only one‐half expressed one or more larger transcripts (8.4, 7.2, and/or 3.0 kb). Autoimmune disease did not correlate with expression of any of the xenotropic transcripts. Xenotropic and MCF transcripts were expressed independently among the mouse strains studied. Splenic RNA from all strains contained 7.2‐, 3.0‐, and 1.8‐kb MCF transcripts. Some strains also expressed 8.4‐kb MCF splenic RNA. There was a strong association between murine lupus and expression of 8.4‐kb MCF transcripts: 6 of 6 lupus‐prone strains, but only 2 of 11 nonautoimmune strains, had detectable 8.4‐kb MCF RNA. The xid and Yaa mutations had minimal effects on expression of 8.4‐kb MCF‐related transcripts, despite their major and opposite effects on disease. Moreover, New Zealand black mice highly expressed this RNA from day 1 of life, before disease development. The data suggest that expression of 8.4‐kb MCF endogenous retroviral transcripts is a primary feature of murine lupus and is not secondary to disease expression.

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“…Indeed, diverse T cell dysfunctions appear to exist independently of the interaction of autoantibody with T lymphocytes (17,18).…”

Section: Systemic Lupus Erythematosus (Sle) Is Characterized By Disormentioning

confidence: 99%

Impaired mobility of human t lymphocyte surface molecules during inactive systemic lupus erythematosus. relationship to a defective camp pathway

Mitchell

1988

Arthritis & Rheumatism

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The T lymphocytes of patients with active systemic lupus erythematosus (SLE) exhibit impaired capping of the surface molecules CD3, CD4, and CDS and a defective CAMP-dependent pathway. Since the mobility of these molecules is regulated in part by CAMP, we sought to determine whether there is a specific defect(s) along the T cell cAMP pathway that contributes to the persistent capping disorder observed during inactive SLE. The data suggest that a defect may exist at the level of CAMP-dependent protein kinase activation or at a point distally. We propose that a disorder of CAMPdependent protein kinase activity might account for the defect of capping observed in both the CD3,CD4 (helperlinducer) and CD3,CDS (suppressor) subsets observed in SLE. (2-14), the genesis of the aberrant immune response remains uncertain. It has been demonstrated that autoantibodies directed against cell surface molecules of mononuclear cells can modify the immune response in SLE by interfering with interactions between cells (15). Systemic lupus erythematosus (SLE) is characterized by disordered humoral and cellular immunity ( I ) . Although several functional immune defects of mononuclear cells have been identified

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T cell abnormalities in NZB mice occur independently of autoantibody production.

Cited by 71 publications

References 45 publications

Ability of the xid gene to prevent autoimmunity in (NZB X NZW)F1 mice during the course of their natural history, after polyclonal stimulation, or following immunization with DNA.

Ability of the xid gene to prevent autoimmunity in (NZB X NZW)F1 mice during the course of their natural history, after polyclonal stimulation, or following immunization with DNA.

Expression of an endogenous retroviral transcript is associated with murine lupus

Impaired mobility of human t lymphocyte surface molecules during inactive systemic lupus erythematosus. relationship to a defective camp pathway

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