1: J Immunol. 2005 Aug 15;175(4):2102-10. 

Opposing roles for RelB and Bcl-3 in regulation of T-box expressed in T cells,
GATA-3, and Th effector differentiation.

Corn RA, Hunter C, Liou HC, Siebenlist U, Boothby MR.

Department of Microbiology, Meharry Medical College, Nashville, TN 37208, USA.

CD4+ T cells with a block in the NF-kappaB signaling pathway exhibit decreases
in Th1 responses and diminished nuclear levels of multiple transactivating
NF-kappaB/Rel/IkappaB proteins. To determine the lineage-intrinsic contributions
of these transactivators to Th differentiation, T cells from mice deficient in
specific subunits were cultured in exogenous cytokines promoting either Th1 or
Th2 differentiation. RelB-deficient cells exhibited dramatic defects in Th1
differentiation and IFN-gamma production, whereas no consistent defect in either
Th1 or Th2 responses was observed with c-Rel-deficient cells. In sharp contrast,
Bcl-3-null T cells displayed no defect in IFN-gamma production, but their Th2
differentiation and IL-4, IL-5, and IL-13 production were significantly
impaired. The absence of RelB led to a dramatic decrease in the expression of
T-box expressed in T cells and Stat4. In contrast, Bcl-3-deficient cells
exhibited decreased GATA-3, consistent with evidence that Bcl-3 can
transactivate a gata3 promoter. These data indicate that Bcl-3 and RelB exert
distinct and opposing effects on the expression of subset-determining
transcription factors, suggesting that the characteristics of Th cell responses
may be regulated by titrating the stoichiometry of transactivating
NF-kappaB/Rel/IkappaB complexes in the nuclei of developing helper effector
cells.

PMID: 16081776 [PubMed - in process]


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2: Immunobiology. 2000 Nov;202(4):394-407. 

Erratum in:
    Immunobiology 2001 May;203(4):705. Vogel F [corrected to Vogl F].

Dendritic cells conditionally transformed by v-relER oncogene express lymphoid
marker genes.

Madruga J, Briegel K, Diebold S, Boehmelt G, Vogl F, Zenke M.

Max-Delbruck-Center for Molecular Medicine, Berlin, Germany.

The initiation of primary immune responses is the key function of specialized
antigen presenting cells, the dendritic cells (DC). DC of myeloid origin capture
antigens in tissues, migrate to lymphoid organs and stimulate T cell responses.
A subset of DC has been described which expresses lymphoid determinants and has
potential regulatory functions. Conditional transformation of chicken bone
marrow progenitors with v-relER, a v-rel estrogen receptor (ER) fusion gene,
allows expansion of progenitors that can be induced to differentiate into DC in
vitro. In this paper we describe that v-relER cells exhibit both myeloid and
lymphoid surface markers, while B cell, T cell and NK (natural killer)-specific
surface markers are absent. v-relER DC express, however, cytoplasmic CD3 protein
and mRNA for CD8alpha and the lymphoid transcription factor GATA-3. These data
suggest that v-relER DC might be related to the lymphoid subset of DC described
in mammals.

PMID: 11131155 [PubMed - indexed for MEDLINE]


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3: Annu Rev Immunol. 1999;17:149-87. 

Transcriptional regulation of T lymphocyte development and function.

Kuo CT, Leiden JM.

Department of Medicine, University of Chicago, Illinois 60637, USA.

The development and function of T lymphocytes are regulated tightly by signal
transduction pathways that include specific cell-surface receptors,
intracellular signaling molecules, and nuclear transcription factors. Since
1988, several families of functionally important T cell transcription factors
have been identified. These include the Ikaros, LKLF, and GATA3 zinc-finger
proteins; the Ets, CREB/ATF, and NF-kappa B/Rel/NFAT transcription factors; the
Stat proteins; and HMG box transcription factors such as LEF1, TCF1, and Sox4.
In this review, we summarize our current understanding of the transcriptional
regulation of T cell development and function with particular emphasis on the
results of recent gene targeting and transgenic experiments. In addition to
increasing our understanding of the molecular pathways that regulate T cell
development and function, these results have suggested novel targets for genetic
and pharmacological manipulation of T cell immunity.

Publication Types:
    Review

PMID: 10358756 [PubMed - indexed for MEDLINE]


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