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T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Isolation and Th17 Differentiation of Na&iuml;ve CD4 T Lymphocytes
12:59

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Published on: September 26, 2013

Pathogen-induced inflammatory environment controls effector and memory CD8+ T cell differentiation.

Joshua J Obar1, Evan R Jellison, Brian S Sheridan

  • 1Center for Integrated Immunology and Vaccine Research, Department of Immunology, University of Connecticut Health Center, Farmington, CT 06030, USA. joshua.obar@montana.edu

Journal of Immunology (Baltimore, Md. : 1950)
|October 12, 2011
PubMed
Summary

Viral and bacterial infections induce distinct CD8(+) T cell differentiation pathways. CpG-DNA stimulation enhances CD8(+) T cell responses, influencing effector and memory cell populations differently depending on context.

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Area of Science:

  • Immunology
  • Cellular Biology
  • Infectious Disease

Background:

  • CD8(+) T cells proliferate exponentially upon infection, differentiating into short-lived effector cells (SLECs) and memory precursor effector cells.
  • The differentiation pathways of CD8(+) T cells vary depending on the type of pathogen and the priming context.

Purpose of the Study:

  • To investigate the differences in CD8(+) T cell differentiation during viral (vesicular stomatitis virus) versus bacterial (Listeria monocytogenes) infections.
  • To determine the role of Ebi3 in SLEC generation.
  • To explore the effects of CpG-DNA administration on CD8(+) T cell differentiation and functionality, including the involvement of IL-12.

Main Methods:

  • Comparative analysis of CD8(+) T cell differentiation during vesicular stomatitis virus and Listeria monocytogenes infections.
  • Assessment of SLEC generation dependence on Ebi3 expression.
  • Investigation of CpG-DNA effects on CD8(+) T cell responses, including IL-12 dependency.
  • Analysis of CD8(+) T cell population dynamics during secondary immune responses.

Main Results:

  • CD8(+) T cell differentiation into SLECs was significantly reduced during vesicular stomatitis virus infection compared to Listeria monocytogenes infection.
  • SLEC generation was dependent on Ebi3 expression.
  • CpG-DNA administration enhanced SLEC differentiation during vesicular stomatitis virus infection via an IL-12-dependent mechanism.
  • CpG-DNA treatment improved effector CD8(+) T cell function and memory subset distribution independently of IL-12.
  • Secondary CD8(+) T cell responses showed increased SLEC accumulation and novel CD127(high)KLRG1(high) memory cells, which persisted but were less effective in recall than memory precursors.

Conclusions:

  • The context of T cell priming significantly alters downstream effector and memory CD8(+) T cell differentiation.
  • Ebi3 is crucial for SLEC generation.
  • CpG-DNA can modulate CD8(+) T cell responses, with distinct IL-12-dependent and independent effects on differentiation and functionality.
  • Novel memory subsets arise during secondary responses, highlighting the plasticity of the CD8(+) T cell memory pool.