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Departments of
*
Dermatology and Allergology and
Neurology, Hannover Medical University, Hannover, Germany; and
Department of Immunology, Georg-August-University, Göttingen, Germany
The C3a molecule is an anaphylatoxin of the C system with a wide
spectrum of proinflammatory effects predominantly on cells of myeloid
origin. In this study we investigated the expression of the high
affinity receptor for C3a (C3aR) in human T lymphocytes using
receptor-specific mAb. C3aR expression was detected in CD4+
and CD8+ blood- or skin-derived T cell clones (TCC) from
birch pollen-sensitized patients with atopic dermatitis. No significant
difference in C3aR expression in CD4+ or CD8+
TCCs could be observed. In contrast to C3a(desArg), C3a led to a
transient calcium flux in TCCs expressing the C3aR, whereas
C3aR-negative TCCs were unreactive. Circulating T cells from patients
suffering from severe inflammatory skin diseases expressed the C3aR,
whereas no expression of C3aR could be found in unstimulated T
lymphocytes from patients with mild inflammatory skin diseases or from
healthy individuals. Type I IFNs, which are potent stimulators of
cellular immunity, were identified as up-regulators of C3aR expression
in vitro in freshly isolated or cloned T lymphocytes. Moreover,
C3aR+ T cells were found at the sites of injection in
IFN-
-treated patients with multiple sclerosis. These data provide
direct evidence for the expression of C3aR on activated human T
lymphocytes; this may point to a biological function of C3a in T
cell-dependent diseases.
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