Clonal Analysis of Peripheral T Cell Precursors in Ipr Mice
作者:
CroghanThomas W.,
RapaportRebecca,
FrelingerJeffrey S.,
EisenbergRobert A.,
CohenPhilip L.,
期刊:
Autoimmunity
(Taylor Available online 1992)
卷期:
Volume 12,
issue 4
页码: 295-302
ISSN:0891-6934
年代: 1992
DOI:10.3109/08916939209148472
出版商: Taylor&Francis
关键词: Ipr;autoimmunity;T cell;triple negative;MRL
数据来源: Taylor
摘要:
MRL/Mp-lpr/lpr mice develop massive lymphadenopathy characterized by expansion of an unusual population of T cells with the Thy 1+, CD3+, CD4-, CD8-(double negative) phenotype. The role these cells play in accelerating the autoimmune syndrome seen in these mice is unknown. In order to better understand the origin of the expanded population of T cells, we have derived a panel hybridomas from double negativeIprlymph node cells. Surprisingly, eleven of twelve hybridomas selected for the absence of surface CD4 and CD8 do not express CD3. Six of eleven confirmed to have inherited the MRL T cell receptor locus have rearrangement at that locus, suggesting commitment to a T cell lineage. Only hybridoma 2.4, which expresses CD3, responds to ConA, anti-CD3 monoclonal antibody, and induces antibody production. The presence of CD3-, CD4-, CD8-T cells in the periphery ofIprmice confirms aberrant T cell development in these mice and suggests an intrinsic cell defect which is expressed early in lymphopoiesis.
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