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A major histocompatibility complex class I-dependent subset of memory phenotype CD8+ cells

Onur Boyman1, Jae-Ho Cho, Joyce T Tan

  • 1Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037, USA.

The Journal of Experimental Medicine
|July 5, 2006
PubMed

Insights

Most CD8(+) T cells with memory phenotype (MP) are IL-15 dependent. However, a distinct CD122(lo) MP CD8(+) subset is controlled by MHC class I molecules, resembling antigen-dependent memory cells.

Area of Science:

  • Immunology
  • T cell biology
  • Cellular immunology

Background:

  • Most CD8(+) T cells with a memory phenotype (MP) are IL-15 dependent and express high levels of CD122.
  • A subset of MP CD8(+) T cells exhibits low CD122 expression (CD122(lo)) and IL-15 independence.

Purpose of the Study:

  • To investigate the regulatory mechanisms controlling the CD122(lo) subset of memory phenotype CD8(+) T cells.
  • To characterize the phenotype and function of CD122(lo) MP CD8(+) T cells.

Main Methods:

  • Flow cytometry analysis of T cell surface markers (CD44, CD122, CD62L, CD69, CD43, CD127).
  • Studies in genetically modified mice (common gamma chain-deficient and MHC class I-deficient mice).
  • Adoptive transfer experiments to assess cell survival and proliferation in different host environments.

Main Results:

  • The CD122(lo) MP CD8(+) T cell subset is primarily regulated by Major Histocompatibility Complex (MHC) class I molecules.
  • These cells display markers of recent activation (CD62L(lo), CD69(hi), CD43(hi), CD127(lo)) and exhibit high background proliferation.
  • CD122(lo) MP CD8(+) T cells are enriched in common gamma chain-deficient mice and absent in MHC-I(-/-) mice.
  • Their survival and proliferation are impaired in MHC-I(-/-) hosts.

Conclusions:

  • The CD122(lo) MP CD8(+) T cell population represents a distinct lineage controlled by MHC class I.
  • These cells share functional similarities with antigen-dependent memory CD8(+) T cells observed during chronic viral infections.
  • This finding expands our understanding of CD8(+) T cell memory heterogeneity and regulation.

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