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Citations to this article

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.
B J Steinberg, … , K Frederiksen, A D Steinberg
B J Steinberg, … , K Frederiksen, A D Steinberg
Published September 1, 1982
Citation Information: J Clin Invest. 1982;70(3):587-597. https://doi.org/10.1172/JCI110651.
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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.

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Abstract

F1 hybrid offspring of New Zealand Black mothers and New Zealand White fathers [(NZB X NZW)F1] female mice develop antibodies to single-stranded (ss) and native DNA, immune complex glomerulonephritis, massive proteinuria, and premature death with renal failure. By a series of matings, congenic (NZB X NZW)F1 . xid/xid mice were prepared. These mice were different from (NZB X NZW)F1 mice in having the X chromosome-linked immune deficiency gene, xid, in homozygous form. Such congenic (NZB X NZW)F1 . 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)F1]. 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)F1 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. The xid/xid mice failed to produce anti-ssDNA following immunization with ssDNA complexed to a protein carrier in fluid form or even emulsified in adjuvant. Finally, the xid/xid mice failed to produce antiDNA in response to multiple injections of the polyclonal activator, bacterial lipopolysaccharide (LPS), or the polyclonal activator, polyribose inosinic acid . polyribose cytidylic acid. However, the xid/xid mice were neither generally hyporesponsive nor unable to recognize LPS because they made normal antibody responses following immunization with LPS to which multiple trinitrophenyl groups were chemically attached. We conclude from these studies that xid/xid, which is known to cause the deletion of a B cell subset, has a profound affect upon (NZB X NZW)F1 mice, rendering them insusceptible to the naturally occurring autoimmune disease characteristic of (NZB X NZW)F1 mice, and preventing them from producing antibodies to DNA despite purposeful immunization and polyclonal B cell activation. These results force a reevaluation of previous concepts regarding the mechanisms by which xid/xid might interfere with the development of autoimmunity, and a consideration of therapeutic implications.

Authors

B J Steinberg, P A Smathers, K Frederiksen, A D Steinberg

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RT Steinberg, ML Miller, AD Steinberg
Clinical Immunology and Immunopathology 1985
Polyclonal B-cell activation in SLE: Frequencies of autoantibody secreting cells
R Dziarski
Clinical Immunology Newsletter 1985
A Large Deletion Within the T-Cell Receptor Beta-Chain Gene Complex in New Zealand White Mice
BL Kotzin, VL Barr, E Palmer
Science 1985
Differential gene expression in autoimmune mice
J D Mountz, J F Mushinski, A D Steinberg
Survey of immunologic research 1985
B Cell-Tropic Interleukins in Murine Systemic Lupus Erythematosus (SLE) 1
GJ Prud-Homme, TM Fieser, FJ Dixon&, AN Theoflopoulos
Immunological Reviews 1984
Opposing effects of xid and nu mutations on proliferative and polyclonal antibody and autoantibody responses to peptidoglycan, LPS, protein A and PWM
R Dziarski
Immunology 1984
Abrogation of murine lupus by the xid gene is associated with reduced responsiveness of B cells to T-cell-helper signals
TM Fieser, ME Gershwin, AD Steinberg, FJ Dixon, AN Theofilopoulos
Cellular Immunology 1984
Cloning of B cells from autoimmune MRL-lpr/lpr and MRL.xid mice
DS Pisetsky, SA Caster, M Piper, DW Scott, AD Steinberg
Cellular Immunology 1984
Studies of immune defective mice
JD Mountz, ES Raveche, PD Noguchi, AD Steinberg
Clinical Immunology and Immunopathology 1984
Recent advances in SLE
JD Mountz, AD Steinberg
Clinical Immunology Newsletter 1984
Induction of murine autoimmune disease by chronic polyclonal B cell activation
L Hang, JH Slack, C Amundson, S Izui, AN Theofilopoulos, FJ Dixon
Journal of Experimental Medicine 1983
B-cell hyperactivity in murine lupus II. Defects in response to and production of accessory signals in lupus-prone mice
AN Theofilopoulos, GJ Prud'homme, TM Fieser, FJ Dixon
Immunology Today 1983
Effect of xid on anti-DNA B-cell precursors
DS Pisetsky, SA Caster, AD Steinberg
Cellular Immunology 1983

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