title: Activated human T lymphocytes express a functional C3a receptor.
abstract: 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-beta-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.
authors.affiliation: Department of Dermatology, Hannover Medical University, Hannover, Germany. Thomas_Werfel@t-online.de
authors.forename: T
authors.initials: T
authors.lastname: Werfel
authors.forename: K
authors.initials: K
authors.lastname: Kirchhoff
authors.forename: M
authors.initials: M
authors.lastname: Wittmann
authors.forename: G
authors.initials: G
authors.lastname: Begemann
authors.forename: A
authors.initials: A
authors.lastname: Kapp
authors.forename: F
authors.initials: F
authors.lastname: Heidenreich
authors.forename: O
authors.initials: O
authors.lastname: Götze
authors.forename: J
authors.initials: J
authors.lastname: Zwirner
mesh_terms: D000911:Antibodies, Monoclonal / Q000378:metabolism; D002469:Cell Separation; D002999:Clone Cells; D015926:Complement C3a / Q000378:metabolism*; D003876:Dermatitis, Atopic / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007111:Immunity, Cellular; D007113:Immunity, Innate; D007370:Interferon Type I / Q000494:pharmacology; D008213:Lymphocyte Activation / Q000276:immunology*; D008565:Membrane Proteins; D011951:Receptors, Complement / Q000096:biosynthesis* / Q000276:immunology / Q000502:physiology; D012867:Skin / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D013601:T-Lymphocytes / Q000276:immunology* / Q000378:metabolism*
chemical_list: D000911:Antibodies, Monoclonal; D007370:Interferon Type I; D008565:Membrane Proteins; D011951:Receptors, Complement; C085567:complement C3a receptor; D015926:Complement C3a