Deficient interleukin 2 activity in MRL/Mp and C57BL/6J mice bearing the lpr gene

Spleen cells from MRL-lpr and B6-lpr mice have a marked defect in the ability to produce interleukin 2 (IL-2) in response to concanavalin A stimulation. This defect precedes the onset of clinical illness, increases with age, and eventually becomes virtually absolute. It is not due to cellular suppre...

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Bibliographic Details
Published inThe Journal of experimental medicine Vol. 154; no. 5; pp. 1671 - 1680
Main Authors Wofsy, D, Murphy, E D, Roths, J B, Dauphinée, M J, Kipper, S B, Talal, N
Format Journal Article
LanguageEnglish
Published United States The Rockefeller University Press 01.11.1981
Subjects
Absorption
Animals
Autoimmune Diseases - etiology
Autoimmune Diseases - genetics
Autoimmune Diseases - pathology
Interleukin-2 - biosynthesis
Interleukin-2 - deficiency
Interleukin-2 - pharmacology
Lymphocyte Activation
Lymphokines - deficiency
Mice
Mice, Inbred C57BL
Spleen - cytology
Spleen - immunology
T-Lymphocytes - immunology
Tetradecanoylphorbol Acetate - pharmacology
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Summary:Spleen cells from MRL-lpr and B6-lpr mice have a marked defect in the ability to produce interleukin 2 (IL-2) in response to concanavalin A stimulation. This defect precedes the onset of clinical illness, increases with age, and eventually becomes virtually absolute. It is not due to cellular suppression of IL-2 production, nor does it reflect the presence of a soluble inhibitor of IL-2 activity. Failure to restore IL-2 production with macrophage-replacing factors, such as interleukin 1 and phorbol myristic acetate, suggests that IL-2 deficiency reflects a primary T cell defect rather than a macrophage defect. MRL-lpr and B6-lpr spleen cells also have an age-dependent reduction in IL-2 response that apparently results from a deficiency of cell surface receptors for IL-2. Congenic MRL-+/+ and B6-+/+ mice, which lack the lpr gene responsible for accelerated autoimmunity and lymphoproliferation, have normal IL-2 activity. These findings suggest that a defect in IL-2 activity may contribute to impaired immunoregulation in mice bearing the lpr gene. The absence of such a defect in MRL-+/+ and B6-+/+ mice further suggests that a single autosomal recessive gene is responsible for IL-2 deficiency.
ISSN:0022-1007
1540-9538
DOI:10.1084/jem.154.5.1671