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Opposing signals from the Bcl6 transcription factor and the interleukin-2 receptor generate T helper 1 central and

Marion Pepper1, Antonio J Pagán, Botond Z Igyártó

  • 1Department of Microbiology, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA.

Immunity
|October 25, 2011
PubMed

Insights

Listeria monocytogenes infection forms distinct CD4(+) T cell populations. These early effector cells differentiate into T helper 1 (Th1) effector memory and follicular helper-like central memory cells.

Area of Science:

  • Immunology
  • Microbial Pathogenesis

Background:

  • Listeria monocytogenes infection induces T helper 1 (Th1) effector memory cells.
  • CC chemokine receptor 7 (CCR7)(+) cells exhibit characteristics of central memory cells.

Purpose of the Study:

  • To track endogenous L. monocytogenes-specific CD4(+) T cells.
  • To elucidate the formation pathways of distinct memory T cell populations.

Main Methods:

  • Tracking of L. monocytogenes-specific CD4(+) T cells post-infection.
  • Analysis of effector cell populations based on transcription factor expression (T-bet, Bcl6) and surface markers (CCR7, CXCR5).

Main Results:

  • Two distinct early effector CD4(+) T cell populations were identified.
  • One population expressed T-bet, leading to Th1 memory cells dependent on the interleukin-2 (IL-2) receptor.
  • The second population expressed CCR7, CXCR5, Bcl6, and depended on inducible costimulator ligand on B cells, generating follicular helper-like memory cells.

Conclusions:

  • Early effector CD4(+) T cells diverge into distinct lineages.
  • Differentiation is influenced by signals from the IL-2 receptor, Bcl6, and B cells.
  • This divergence results in the generation of both Th1 effector memory and follicular helper-like central memory cells.

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