References
Query Results -- Details
MGI Accession ID: MGI:55112
J Number: J:6638
Other Accession IDs:
Title: Deficient interleukin 2 activity in MRL/Mp and C57BL/6J mice bearing the lpr gene.
Authors: Wofsy D; Murphy ED; Roths JB; Dauphinee MJ; Kipper SB; Talal N
Journal: J Exp Med
Volume: 154
Issue: 5
Date: 1981 Nov 1
Year: 1981
Pages: 1671-80
Review Status: Peer Reviewed
Abstract:
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.
Additional Information:
