Different immunological mechanisms govern protection from experimental stroke in young and older mice with recombinant TCR ligand therapy

Abby L. Dotson, Wenbin Zhu, Nicole Libal, Nabil Alkayed, Halina Offner

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Stroke is a leading cause of death and disability in the United States. The lack of clinical success in stroke therapies can be attributed, in part, to inadequate basic research on aging rodents. The current study demonstrates that recombinant TCR ligand therapy uses different immunological mechanisms to protect young and older mice from experimental stroke. In young mice, RTL1000 therapy inhibited splenocyte efflux while reducing frequency of T cells and macrophages in the spleen. Older mice treated with RTL1000 exhibited a significant reduction in inflammatory cells in the brain and inhibition of splenic atrophy. Our data suggest age specific differences in immune response to stroke that allow unique targeting of stroke immunotherapies.

Original languageEnglish (US)
Pages (from-to)1-13
Number of pages13
JournalFrontiers in Cellular Neuroscience
Volume8
Issue numberSEP
DOIs
StatePublished - 2014

Fingerprint

Stroke
Ligands
Therapeutics
Immunotherapy
Atrophy
Cause of Death
Rodentia
Spleen
Macrophages
T-Lymphocytes
Brain
Research

Keywords

  • Aging
  • Experimental stroke
  • Immune response
  • Neuroinflammation
  • RTL1000
  • Therapy

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience

Cite this

Different immunological mechanisms govern protection from experimental stroke in young and older mice with recombinant TCR ligand therapy. / Dotson, Abby L.; Zhu, Wenbin; Libal, Nicole; Alkayed, Nabil; Offner, Halina.

In: Frontiers in Cellular Neuroscience, Vol. 8, No. SEP, 2014, p. 1-13.

Research output: Contribution to journalArticle

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