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Abrogation of CCL21 chemokine function by transgenic over-expression impairs T cell immunity to local infections

Heike Unsoeld1, Katja Mueller, Ulrike Schleicher

  • 1Department of Immunology, Institute of Medical Microbiology and Hygiene, University of Freiburg, Freiburg, Germany.

International Immunology
|October 5, 2007
PubMed

Insights

The CC chemokine receptor 7 (CCR7) pathway is crucial for T cell immunity against local infections. Impaired CCR7 signaling in transgenic mice reduced T cell responses to viral and parasitic pathogens after footpad infection.

Area of Science:

  • Immunology
  • Cell Biology
  • Virology

Background:

  • CC chemokine receptor 7 (CCR7) and its ligands CCL21/CCL19 are vital for immune cell trafficking to lymphoid organs.
  • Understanding CCR7's role in T cell-mediated immunity against pathogens is essential.

Purpose of the Study:

  • To investigate the in vivo function of CCR7 in T cell immunity against infectious agents.
  • To analyze the impact of altered CCL21 levels on T cell migration and immune responses.

Main Methods:

  • Generation of transgenic (tg) mice ubiquitously expressing CCL21.
  • Assessment of T cell migration in vitro and immune responses to lymphocytic choriomeningitis virus and Leishmania major in vivo.
  • Analysis of lymph node structure and cell distribution.

Main Results:

  • Transgenic mice exhibited high serum CCL21, leading to CCR7 down-regulation and impaired T cell migration in vitro.
  • Lymph nodes were smaller but structurally normal with preserved T and B cell distribution.
  • CD8 T cell response to footpad infection with lymphocytic choriomeningitis virus was decreased, while systemic infection response was unaffected.
  • CD4 T cell response to Leishmania major footpad infection was reduced, with impaired parasite clearance.

Conclusions:

  • CCR7 signaling is critical for effective T cell-mediated immunity following local viral and parasitic infections.
  • Altered CCR7 ligand expression significantly impacts T cell responses at the site of infection.

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