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Updated: Jul 12, 2026

Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice
07:17

Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice

Published on: June 22, 2016

CD22 is upregulated and displays suppressive properties on CD4+ T cells upon a persistent virus infection

Ying He1,2, Vijayamahantesh Vijayamahantesh1,2, Lei Jiang3

  • 1Department of Surgery, University of Missouri, Columbia, MO, United States.

Journal of Immunology (Baltimore, Md. : 1950)
|July 11, 2026
PubMed

Insights

Sphingosine kinase 2 (SphK2) upregulates CD22 on T cells during chronic lymphocytic choriomeningitis virus (LCMV) infection, suppressing immune responses. This SphK2-CD22 pathway offers insights into viral immune evasion.

Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Chronic viral infections often suppress host immunity, with mechanisms incompletely understood.
  • Sphingosine kinase 2 (SphK2) was previously shown to repress CD4+ T-cell immunity during lymphocytic choriomeningitis virus (LCMV) Clone 13 infection.

Purpose of the Study:

  • To investigate the role of CD22 in viral immune suppression during LCMV infection.
  • To elucidate the relationship between SphK2 and CD22 in regulating T-cell responses to chronic viral infections.

Main Methods:

  • Analysis of CD22 expression on virus-specific T cells during LCMV infection.
  • Assessment of T-cell responses following transient or complete CD22 deletion.
  • Adoptive transfer experiments using CD22-deficient T-cell receptor transgenic T cells.
  • Gene signature profiling of LCMV-specific CD4+ T cells.

Main Results:

  • CD22 is significantly upregulated on virus-specific T cells during LCMV infection, dependent on SphK2.
  • CD22 upregulation is sustained during persistent LCMV Cl 13 infection.
  • Complete CD22 deletion did not significantly affect T-cell immunity, suggesting compensatory mechanisms, while transient depletion showed modest enhancement.
  • CD22-deficient T cells exhibited enhanced expansion and improved functionality compared to CD22-sufficient cells, indicating an intrinsic suppressive function.

Conclusions:

  • CD22 plays a CD4+ T cell-intrinsic suppressive role during LCMV infection.
  • The SphK2-CD22 axis is a key regulator of CD4+ T-cell immunity during viral infections.
  • Understanding this axis can advance knowledge of viral immune suppression and persistence.
Keywords:
CD22LCMVT-cell suppressionsphingosine kinase 2viral persistence

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