International Immunology, Vol 9, 1243-1251, Copyright © 1997 by Oxford University Press
L Nagelkerken, B Blauw and M Tielemans
IL-10 and IL-4 were studied with respect to their capacity to inhibit
experimental allergic encephalomyelitis (EAE) induced in SJL/J mice by
immunization with the proteolipid protein peptide PLP139-151. Treatment
with 2 micrograms IL-10/day from day 0 until day 12 delayed onset of
disease and inhibited the severity of EAE. By contrast, a daily dose of 0.5
microgram IL-4 was ineffective. Instead of acting in a synergistic fashion,
IL-4 even abrogated the inhibitory effect of IL-10. The effects of IL-10
and IL-4 treatment were largely consistent with the (lack of) ability of
these cytokines to down-regulate the inflammatory response in brain tissue.
Although IL-4 was ineffective in the inhibition of EAE, lymph node cells
from IL-4-treated mice displayed a strongly inhibited peptide-specific
IFN-gamma production. By contrast, IL-10, which was effective in inhibiting
EAE, showed no significant inhibition of IFN-gamma at this level. Neither
cytokine treatment resulted in detectable levels of peptide-specific IL-4.
Indirect evidence for the activity of Th2 cells in vivo came from the
observation that IL-10 inhibited the primary PLP139-151-specific IgG2a and
IgG3 response in favor of IgG1, whereas IL-4 inhibited the primary antibody
response to the peptide, regardless of subclass. The combination of IL-4
and IL-10 did not affect the subclass composition. The observation that
IL-10-treated mice remained sensitive to re- induction of EAE is not in
support of an important role of Th2 cells in regulating disease activity in
this model of actively induced EAE.
ARTICLES
IL-4 abrogates the inhibitory effect of IL-10 on the development of experimental allergic encephalomyelitis in SJL mice [published erratum appears in Int Immunol 1997 Nov;9(11):1773]
Division of Immunological and infectious Diseases, TNO Prevention and Health, Leiden, The Netherlands.
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