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Related Experiment Videos

Activated human T lymphocytes express a functional C3a receptor.

T Werfel1, K Kirchhoff, M Wittmann

  • 1Department of Dermatology, Hannover Medical University, Hannover, Germany. Thomas_Werfel@t-online.de

Journal of Immunology (Baltimore, Md. : 1950)
|November 22, 2000
PubMed
Summary

The complement system

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Area of Science:

  • Immunology
  • Cell Biology
  • Complement System

Background:

  • The complement system molecule C3a (anaphylatoxin) has broad pro-inflammatory effects, primarily on myeloid cells.
  • The expression and function of C3a's high-affinity receptor (C3aR) on human T lymphocytes remain largely uncharacterized.
  • Understanding C3aR expression on T cells is crucial for elucidating C3a's role in T cell-mediated inflammatory diseases.

Purpose of the Study:

  • To investigate the expression of the C3a receptor (C3aR) on human T lymphocytes.
  • To determine the functional consequences of C3a binding to T cells.
  • To explore the regulation of C3aR expression and its presence in inflammatory conditions.

Main Methods:

  • Utilized receptor-specific monoclonal antibodies (mAbs) to detect C3aR expression.

Related Experiment Videos

  • Analyzed C3aR expression on T cell clones (TCCs) from allergic patients and circulating T cells from patients with inflammatory skin diseases.
  • Assessed C3a-induced calcium flux in TCCs and investigated the effect of Type I Interferons (IFNs) on C3aR expression in vitro.

    • Main Results:

    • C3aR was detected on activated CD4(+) and CD8(+) T cell clones (TCCs) from patients with atopic dermatitis.
    • C3a induced a transient calcium flux in C3aR-expressing TCCs, indicating functional receptor activity.
    • C3aR was found on circulating T cells in severe inflammatory skin diseases and IFN-beta-treated multiple sclerosis patients, but not in healthy individuals or mild disease cases.

    Conclusions:

    • This study provides direct evidence for C3a receptor (C3aR) expression on activated human T lymphocytes.
    • C3aR expression on T cells is associated with inflammatory conditions and can be upregulated by Type I IFNs.
    • These findings suggest a potential biological role for C3a in T cell-dependent inflammatory diseases.