Abstract:
:IL-12 is a potent inducer of IFN-gamma production and drives the development of Th1 cells. Human polarized Th2 cells do not express the signaling beta2-subunit of the IL-12R and, therefore, do not signal in response to IL-12. The question was raised as to what extent the loss of the IL-12Rbeta2 chain in Th2 cells has bearing on the stability of the human Th2 phenotype. In the present report, we show that restimulation of human fully polarized Th2 cells in the presence of IL-12 primes for a shift towards Th0/Th1 phenotypes, accompanied by suppression of GATA-3 expression and induction of T-bet expression. These reversed cells are further characterized by a marked IL-12Rbeta2 chain expression and fully restored IL-12-inducible STAT4 activation. The IL-12-induced phenotypic shift proved to be stable as a subsequent restimulation in the presence of IL-4 and in the absence of IL-12 could not undo the accomplished changes. Identical results were obtained with cells from atopic patients, both with polyclonal Th2 cell lines and allergen-specific Th2 cell clones. These findings suggest the possibility of restoring IL-12 responsiveness in established Th2 cells of atopic patients by stimulation in the presence of IL-12, and that IL-12-promoting immunotherapy can be beneficial for Th2-mediated immune disorders, targeting both naive and memory effector T cells.
journal_name
Eur J Immunoljournal_title
European journal of immunologyauthors
Smits HH,van Rietschoten JG,Hilkens CM,Sayilir R,Stiekema F,Kapsenberg ML,Wierenga EAdoi
10.1002/1521-4141(200104)31:4<1055::aid-immu1055>3keywords:
subject
Has Abstractpub_date
2001-04-01 00:00:00pages
1055-65issue
4eissn
0014-2980issn
1521-4141pii
10.1002/1521-4141(200104)31:4<1055::AID-IMMU1055>3journal_volume
31pub_type
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