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Updated: Aug 17, 2026

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
Published on: May 8, 2016
Cytokine secretion by deltagamma and alphabeta T cells in monophasic experimental autoimmune encephalomyelitis
M A Jensen1, A Dayal, B G Arnason
1Department of Neurology and the Brain Research Institute, University of Chicago, Chicago, IL 60637, USA. mjensen@drugs.bsd.uchicago.edu
Abstract:
Mononuclear cells were isolated from the central nervous system (CNS), lymph nodes (LN), spleen and blood, over the course of murine monophasic experimental autoimmune encephalomyelitis (EAE). Individual cytokine secreting T cells were enumerated. IL-2-secreting alphabeta T cells were numerous at all sites at disease onset. By disease peak their numbers had fallen profoundly; they remained low thereafter. IL-2 secreting gammadelta T cells were rare throughout. IFN-gamma-secreting cells were plentiful at all sites at disease onset. gammadelta T cells comprised 7% of total and 20% of IFN-gamma-secreting CNS-derived cells at disease onset; values at disease peak were 12 and 40% respectively. IL-4-secreting alphabeta T cells were rare in the CNS and LN throughout and did not increase in the spleen from baseline values. In contrast, splenic IL-4-secreting gammadelta T cells had increased to four-fold baseline values at disease onset and seven-fold at disease peak. Recovery from EAE is associated with a global inhibition of IL-2-secreting alphabeta T cells and to a lesser extent with IFN-gamma-secreting alphabeta and gammadelta T cells, whereas IL-4-secreting gammadelta T cells increase in the spleen as disease evolves.

