T cell clonal anergy
RH Schwartz - Current opinion in immunology, 1997 - Elsevier
RH Schwartz
Current opinion in immunology, 1997•ElsevierRecent experiments have elucidated two molecular mechanisms that may account for the
failure of anergic T cell clones to initiate IL-2 gene transcription following TCR stimulation.
First, a block has been identified in the ERK and JNK mitogen-activated protein kinase
pathways; the block results from a failure to activate p21ras. It leads to reduced induction of c-
Fos and JunB proteins and to a failure to form and phosphorylate the activator protein (AP)-1
heterodimers required for IL-2 gene transcriptional activation. Second, repressor molecules …
failure of anergic T cell clones to initiate IL-2 gene transcription following TCR stimulation.
First, a block has been identified in the ERK and JNK mitogen-activated protein kinase
pathways; the block results from a failure to activate p21ras. It leads to reduced induction of c-
Fos and JunB proteins and to a failure to form and phosphorylate the activator protein (AP)-1
heterodimers required for IL-2 gene transcriptional activation. Second, repressor molecules …
Recent experiments have elucidated two molecular mechanisms that may account for the failure of anergic T cell clones to initiate IL-2 gene transcription following TCR stimulation. First, a block has been identified in the ERK and JNK mitogen-activated protein kinase pathways; the block results from a failure to activate p21ras. It leads to reduced induction of c-Fos and JunB proteins and to a failure to form and phosphorylate the activator protein (AP)-1 heterodimers required for IL-2 gene transcriptional activation. Second, repressor molecules (NiI-2-a and a molecule related to AP-1) have been characterized that dominantly inhibit IL-2 gene transcription.
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