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ß+ CD4-CD8- B220+ Cells Based on High Affinity TCR Signals1
Immunobiology Program, Department of Medicine, University of Vermont College of Medicine, Burlington, VT 05405
The origin of TCR-
ß+
CD4-CD8- cells is unclear, yet accumulating
evidence suggests that they do not represent merely a default pathway
of unselected thymocytes. Rather, they arise by active selection as
evidenced by their absence in mice lacking expression of class I MHC.
TCR-ß+ CD4-CD8- cells also
preferentially accumulate in mice lacking expression of Fas/APO-1/CD95
(lpr) or Fas-ligand (gld), suggesting
that this subset might represent a subpopulation destined for apoptosis
in normal mice. Findings from mice bearing a self-reactive TCR
transgene support this view. In the current study we observe that in
normal mice, TCR-ß+ CD4-CD8-
thymocytes contain a high proportion of cells undergoing apoptosis. The
apoptotic subpopulation is further identified by its expression of B220
and IL2Rß and the absence of surface CD2. The
CD4-CD8- B220+ phenotype is also
enriched in T cells that recognize endogenous retroviral superantigens,
and can be induced in TCR transgenic mice using peptide/MHC complexes
that bear high affinity, but not low affinity, for TCR. A model is
presented whereby the TCR-ß+ CD2-
CD4-CD8- B220+ phenotype arises
from high intensity TCR signals. This model is broadly applicable to
developing thymocytes as well as mature peripheral T cells and may
represent the phenotype of self-reactive T cells that are increased in
certain autoimmune conditions.
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