International Immunology, Vol 9, 1221-1231, Copyright © 1997 by Oxford University Press
LA Diaz Jr, AW Friedman, X He, RD Kuick, SM Hanash and DA Fox
CD98 is a 125 kDa heterodimer, which is strongly expressed on the surface
of activated and proliferating cells. Its expression is strikingly
regulated during T cell differentiation and activation, but the role of
CD98 during T lymphocyte responses is not yet understood. We report here
that proliferation of resting peripheral blood mononuclear cells (PBMC)
induced by lectin, superantigen (SAg) or conventional antigens was blocked
by anti-CD98 heavy chain (CD98hc) mAb. In contrast, anti-CD98hc did not
block responses of T cell clones or lines. Anti-CD98hc inhibited IL-2
receptor expression and progression of T cells from G1 to S phase, but did
not reduce expression of the IL-2 gene. Anti-CD98hc mAb did not regulate
the initial activation events involving the TCR and co-receptor structures,
but instead inhibited T lymphocyte responses even when added 18 h or more
after the activation stimulus. Further experiments demonstrated that
anti-CD98 was not directly affecting T cells in this system, but was
instead acting on accessory cells. This was supported using a novel
xenogeneic system that takes advantage of the lack of xenoreactivity of
purified human T cells against mouse splenocytes. Despite absence of a
direct xenoresponse to murine spleen cells, human T cells were activated by
SAg presented by murine splenic antigen-presenting cells (APC). Murine
anti-human CD98hc did not block T cell proliferation in this system.
Furthermore, responses using monocyte-depleted PBMC as APC were not blocked
by anti-CD98hc. Taken together, the present data suggests that triggering
of human monocyte CD98 can suppress T cell proliferation by a process that
halts progression through the cell cycle of recently activated T
lymphocytes. This may represent a novel pathway for monocyte regulation of
T cell activation.
ARTICLES
Monocyte-dependent regulation of T lymphocyte activation through CD98
Rackham Arthritis Research Unit, Department of Internal Medicine, Specialized Center of Research in Rheumatoid Arthritis, Ann Arbor, MI, USA.
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