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Inability of autoimmune mice with the lpr gene to spontaneously produce interleukin 3

Corresponding Author

Vicki E. Kelley

Laboratory of Immunogenetics and Transplantation, Department of Medicine, Brigham and Women's Hospital, Cambridge, MA

Laboratory of Immunogenetics and Transplantation, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USASearch for more papers by this author

Neal M. Farber,

Neal M. Farber

Charles A. Dana Research Institute, The Harvard-Thorndike Laboratory of the Beth Israel Hospital, Harvard Medical School, Boston and Biogen Research Corp., Cambridge, MA

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John M. Williams,

John M. Williams

Laboratory of Immunogenetics and Transplantation, Department of Medicine, Brigham and Women's Hospital, Cambridge, MA

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Terry B. Strom,

Terry B. Strom

Laboratory of Immunogenetics and Transplantation, Department of Medicine, Brigham and Women's Hospital, Cambridge, MA

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Vicki E. Kelley,

Corresponding Author

Vicki E. Kelley

Laboratory of Immunogenetics and Transplantation, Department of Medicine, Brigham and Women's Hospital, Cambridge, MA

Laboratory of Immunogenetics and Transplantation, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USASearch for more papers by this author

Neal M. Farber,

Neal M. Farber

Charles A. Dana Research Institute, The Harvard-Thorndike Laboratory of the Beth Israel Hospital, Harvard Medical School, Boston and Biogen Research Corp., Cambridge, MA

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John M. Williams,

John M. Williams

Laboratory of Immunogenetics and Transplantation, Department of Medicine, Brigham and Women's Hospital, Cambridge, MA

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Terry B. Strom,

Terry B. Strom

Laboratory of Immunogenetics and Transplantation, Department of Medicine, Brigham and Women's Hospital, Cambridge, MA

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First published: 1986

https://doi.org/10.1002/eji.1830160425

Citations: 5

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Abstract

A recent report (Palacios, R., Eur. J. Immunol. 1984. 14: 599) indicates that spleen cells from MRL-MpJ-lpr/lpr mice spontaneously produce interleukin 3 (IL3) and suggests that this lymphokine could be responsible for promoting the lymphoid hyperplasia regulated by the lpr gene. The present study shows that splenocytes from several murine strains bearing the lpr gene do not spontaneously produce IL3. This has been determined by measuring the amount of this lymphokine by a bioassay and by the detection of IL 3 mRNA using Northern blot analysis. We suggest that another lympbokine is responsible for growth of lymphocytes regulated by the lpr gene.

References

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Volume16, Issue4

1986

Pages 464-467

Inability of autoimmune mice with the lpr gene to spontaneously produce interleukin 3

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Inability of autoimmune mice with the lpr gene to spontaneously produce interleukin 3

Abstract

References

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