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Results: 1 to 4 of 4

Publication Record


CD8αα⁺ innate-type lymphocytes in the intestinal epithelium mediate mucosal immunity.
Van Kaer L, Algood HMS, Singh K, Parekh VV, Greer MJ, Piazuelo MB, Weitkamp JH, Matta P, Chaturvedi R, Wilson KT, Olivares-Villagómez D
(2014) Immunity 41: 451-464
MeSH Terms: Animals, Antigen Presentation, CD8 Antigens, Citrobacter rodentium, Cytochalasin D, Enterocolitis, Necrotizing, Helicobacter pylori, Histocompatibility Antigens Class I, Humans, Immunity, Mucosal, Inhibitor of Differentiation Protein 2, Interleukin Receptor Common gamma Subunit, Interleukin-15, Interleukin-2, Interleukin-7, Intestinal Mucosa, Lymphocyte Activation, Lymphocytes, Mice, Mice, Inbred C57BL, Mice, Knockout, Phagocytosis
Show Abstract · Added January 20, 2015
Innate immune responses are critical for mucosal immunity. Here we describe an innate lymphocyte population, iCD8α cells, characterized by expression of CD8α homodimers. iCD8α cells exhibit innate functional characteristics such as the capacity to engulf and kill bacteria. Development of iCD8α cells depends on expression of interleukin-2 receptor γ chain (IL-2Rγc), IL-15, and the major histocompatibility complex (MHC) class Ib protein H2-T3, also known as the thymus leukemia antigen or TL. While lineage tracking experiments indicated that iCD8α cells have a lymphoid origin, their development was independent of the transcriptional suppressor Id2, suggesting that these cells do not belong to the family of innate lymphoid cells. Finally, we identified cells with a similar phenotype in humans, which were profoundly depleted in newborns with necrotizing enterocolitis. These findings suggest a critical role of iCD8α cells in immune responses associated with the intestinal epithelium.
Copyright © 2014 Elsevier Inc. All rights reserved.
0 Communities
5 Members
0 Resources
22 MeSH Terms
ETO family protein Mtg16 regulates the balance of dendritic cell subsets by repressing Id2.
Ghosh HS, Ceribelli M, Matos I, Lazarovici A, Bussemaker HJ, Lasorella A, Hiebert SW, Liu K, Staudt LM, Reizis B
(2014) J Exp Med 211: 1623-35
MeSH Terms: Animals, Base Sequence, Cell Differentiation, Cell Line, Cell Proliferation, Chromatin, Dendritic Cells, E2F2 Transcription Factor, Gene Deletion, Humans, Inhibitor of Differentiation Protein 2, Mice, Mice, Inbred C57BL, Molecular Sequence Data, Nuclear Proteins, Repressor Proteins, Stem Cells, Transcription Factors
Show Abstract · Added December 8, 2014
Dendritic cells (DCs) comprise two major subsets, the interferon (IFN)-producing plasmacytoid DCs (pDCs) and antigen-presenting classical DCs (cDCs). The development of pDCs is promoted by E protein transcription factor E2-2, whereas E protein antagonist Id2 is specifically absent from pDCs. Conversely, Id2 is prominently expressed in cDCs and promotes CD8(+) cDC development. The mechanisms that control the balance between E and Id proteins during DC subset specification remain unknown. We found that the loss of Mtg16, a transcriptional cofactor of the ETO protein family, profoundly impaired pDC development and pDC-dependent IFN response. The residual Mtg16-deficient pDCs showed aberrant phenotype, including the expression of myeloid marker CD11b. Conversely, the development of cDC progenitors (pre-DCs) and of CD8(+) cDCs was enhanced. Genome-wide expression and DNA-binding analysis identified Id2 as a direct target of Mtg16. Mtg16-deficient cDC progenitors and pDCs showed aberrant induction of Id2, and the deletion of Id2 facilitated the impaired development of Mtg16-deficient pDCs. Thus, Mtg16 promotes pDC differentiation and restricts cDC development in part by repressing Id2, revealing a cell-intrinsic mechanism that controls subset balance during DC development.
© 2014 Ghosh et al.
1 Communities
1 Members
0 Resources
18 MeSH Terms
Myc-mediated transcriptional repression by recruitment of histone deacetylase.
Kurland JF, Tansey WP
(2008) Cancer Res 68: 3624-9
MeSH Terms: Animals, Apoptosis, Cell Cycle Proteins, Cell Proliferation, Chromatin Immunoprecipitation, Gene Expression Regulation, Neoplastic, Histone Deacetylases, Inhibitor of Differentiation Protein 2, Models, Biological, Protein Structure, Tertiary, Proto-Oncogene Proteins c-myc, Rats, Transcription Factor CHOP, Transcription, Genetic
Show Abstract · Added March 10, 2014
Myc is a transcription factor that features prominently in cancer. The oncogenicity of Myc stems from its ability to regulate expression of genes required for cell growth and proliferation. Although the mechanisms through which Myc activates transcription have been extensively studied, less is known about how Myc represses transcription. Recently, we reported that a conserved element within Myc-MbIII- is important for transcriptional repression. Here, we investigate the mechanism through which MbIII contributes to repression. We show that Myc represses transcription of target genes Id2 and Gadd153 by a process that involves histone deacetylation. We show that MbIII is important for repression of these genes and present evidence that this element contributes to repression by recruiting the histone deacetylase HDAC3 to the Id2 and Gadd153 promoters. These results describe a mechanistic role for MbIII in transcription, and reveal that recruitment of HDAC3 is a process by which Myc represses gene activity.
0 Communities
1 Members
0 Resources
14 MeSH Terms
Id2 is dispensable for myc-induced lymphomagenesis.
Nilsson JA, Nilsson LM, Keller U, Yokota Y, Boyd K, Cleveland JL
(2004) Cancer Res 64: 7296-301
MeSH Terms: Animals, B-Lymphocytes, Burkitt Lymphoma, DNA-Binding Proteins, Disease Models, Animal, Female, Inhibitor of Differentiation Protein 2, Male, Mice, Mice, Inbred BALB C, Mice, Knockout, Mice, Transgenic, Proto-Oncogene Proteins c-myc, Repressor Proteins, Transcription Factors
Show Abstract · Added March 5, 2014
The Emu-Myc transgenic mouse appears to be an accurate model of human Burkitt's lymphoma that bears MYC/Immunoglobulin gene translocations. Id2, a negative regulator of basic helix-loop-helix transcription factors, has also been proposed as a Myc target gene that drives the proliferative response of Myc by binding to and overriding the checkpoint functions of the retinoblastoma tumor suppressor protein. Targeted deletion of Id2 in mice results in defects in B-cell development and prevents the development of peripheral lymphoid nodes. In precancerous B cells and lymphomas that arise in Emu-Myc transgenic mice and in Burkitt's lymphomas, Id2 is overexpressed, suggesting that it plays a regulatory role in lymphoma development. Surprisingly, despite these connections, Emu-Myc mice lacking Id2 succumb to lethal B-cell lymphoma at rates comparable with wild-type Emu-Myc transgenics. Furthermore, precancerous splenic B cells lacking Id2 do not exhibit any significant defects in Myc-induced target gene transactivation and proliferation. However, due to their lack of secondary lymph nodes, Emu-Myc mice lacking Id2 rather succumb to disseminated lymphoma with an associated leukemia, with pronounced infiltrates of the bone marrow and other major organs. Collectively these findings argue that targeting Id2 functions may be ineffective in preventing Myc-associated malignancies.
0 Communities
1 Members
0 Resources
15 MeSH Terms