Impairment of intestinal intraepithelial lymphocytes in Id2 deficient mice

Jk, Kim; Takeuchi, Mitsuo; Yokota, Yoshifumi

doi:10.1136/gut.2003.022293

Cited by 18 publications

(14 citation statements)

References 36 publications

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“…Id2, as a non–DNA‐binding protein, inhibits the activity of helix‐loop‐helix transcription factors, especially that of E‐proteins, a family of proteins that are required for normal lymphopoiesis 1, 4. Several studies have indicated that, in normal lymphocytes, Id2 controls activation‐induced cytidine deaminase expression and is crucial for NK‐ or B‐cell development 1, 4, 13, 14, 37. Id2−/− animals have severely reduced numbers of normal, mature NK cells and also lack lymph nodes or Peyer patches.…”

Section: Discussionmentioning

confidence: 99%

The helix‐loop‐helix protein Id2 is expressed differentially and induced by myc in T‐cell lymphomas

Cotta

Leventaki

Atsaves

et al. 2007

Cancer

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BACKGROUND. Inhibitor of DNA binding 2 (Id2), a helix‐loop‐helix protein of the inhibitor of differentiation (ID) family, is involved in hematopoiesis, mainly through interaction with the E‐family of transcription factors. Recent studies have shown that Id2 is overexpressed in some types of B‐cell lymphoma, including classical Hodgkin lymphoma. The authors of the current study hypothesized that Id2 also is overexpressed in T‐cell lymphomas. METHODS. By using reverse‐transcriptase polymerase chain reaction (RT‐PCR) and Western blot analyses, high Id2 messenger RNA (mRNA) and protein levels, respectively, were detected in all 4 T‐cell anaplastic large cell lymphoma (ALCL) cell lines that were tested. RESULTS. Immunohistochemistry results indicated that Id2 was expressed strongly in 21 of 27 (78%) ALCL tumors (79% anaplastic lymphoma kinase [ALK]‐negative and 75% ALK‐positive), in 5 of 10 (50%) extranodal natural killer/T (NK/T)‐cell lymphomas of the nasal type, in 2 of 8 (25%) cutaneous ALCLs, in 2 of 9 (22%) enteropathy type T‐cell lymphomas, in 1 of 5 (20%) peripheral T‐cell lymphomas not otherwise specified, and in 1 of 8 (13%) T‐cell prolymphocytic leukemias. Other types of T‐cell lymphoma were negative for Id2. Because it is known that myc is expressed in ALCL, myc was inhibited selectively in 2 ALCL cell lines, resulting in a concentration‐dependent decrease in Id2 mRNA and protein levels. Conversely, forced expression of myc in HEK 293T cells using an myc/green fluorescent protein adenoviral vector resulted in Id2 up‐regulation. CONCLUSIONS. Taken together, the current data suggest that Id2 commonly is overexpressed in highly proliferative T‐cell lymphomas, and its expression may result from transcriptional activation of myc in these tumors. Cancer 2008. © 2007 American Cancer Society.

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Section: Discussionmentioning

confidence: 99%

The helix‐loop‐helix protein Id2 is expressed differentially and induced by myc in T‐cell lymphomas

Cotta

Leventaki

Atsaves

et al. 2007

Cancer

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“…Besides a lactation defect, mice deficient for Id2 display multiple defects, mainly in the immune system, including agenesis of lymph nodes and Peyer's patches, impaired natural killer cell development (14), selective loss of CD8α + dendritic cells (28,29), Th2 dominance with an increased serum IgE level (28,30) and reduction of intestinal lymphocytes (31). These defects are not observed in C/EBPβ-null mice.…”

Section: Discussionmentioning

confidence: 99%

Regulation of Id2 expression by CCAAT/enhancer binding protein

Karaya

Mori²,

Kimoto³

et al. 2005

Nucleic Acids Research

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Mice deficient for Id2, a negative regulator of basic helix–loop–helix (bHLH) transcription factors, exhibit a defect in lactation due to impaired lobuloalveolar development during pregnancy, similar to the mice lacking the CCAAT enhancer binding protein (C/EBP) β. Here, we show that Id2 is a direct target of C/EBPβ. Translocation of C/EBPβ into the nucleus, which was achieved by using a system utilizing the fusion protein between C/EBPβ and the ligand-binding domain of the human estrogen receptor (C/EBPβ-ERT), demonstrated the rapid induction of endogenous Id2 expression. In reporter assays, transactivation of the Id2 promoter by C/EBPβ was observed and, among three potential C/EBPβ binding sites found in the 2.3 kb Id2 promoter region, the most proximal element was responsible for the transactivation. Electrophoretic mobility shift assay (EMSA) identified this element as a core sequence to which C/EBPβ binds. Chromatin immunoprecipitation (ChIP) furthermore confirmed the presence of C/EBPβ in the Id2 promoter region. Northern blotting showed that Id2 expression in C/EBPβ-deficient mammary glands was reduced at 10 days post coitus (d.p.c.), compared with that in wild-type mammary glands. Thus, our data demonstrate that Id2 is a direct target of C/EBPβ and provide insight into molecular mechanisms underlying mammary gland development during pregnancy.

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“…ID2 was identified as an early marker of innate T cells, preferentially expressed in thymic and bone marrow NK progenitors (144, 145) and other αβTCR + T cells with preprogrammed effector function such as CD8αα + T cells (146, 147) and iNKT cells (148). In TCR + ILE cells, ID2 functions in concert with ID3, but its impact is often constrained to cell maintenance (75, 76, 149).…”

Section: Tf Network Overseeing Innate Lymphoid Lineage Specificitymentioning

confidence: 99%

Transcription Factor Networks Directing the Development, Function, and Evolution of Innate Lymphoid Effectors

Kang

Malhotra

2015

Annu. Rev. Immunol.

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Mammalian lymphoid immunity is mediated by fast and slow responders to pathogens. Fast innate lymphocytes are active within hours after infections in mucosal tissues. Slow adaptive lymphocytes are conventional T and B cells with clonal antigen receptors that function days after pathogen exposure. A transcription factor (TF) regulatory network guiding early T cell development is at the core of effector function diversification in all innate lymphocytes, and the kinetics of immune responses is set by developmental programming. Operational units within the innate lymphoid system are not classified by the types of pathogen-sensing machineries but rather by discrete effector functions programmed by regulatory TF networks. Based on the evolutionary history of TFs of the regulatory networks, fast effectors likely arose earlier in the evolution of animals to fortify body barriers, and in mammals they often develop in fetal ontogeny prior to the establishment of fully competent adaptive immunity.

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Impairment of intestinal intraepithelial lymphocytes in Id2 deficient mice

Cited by 18 publications

References 36 publications

The helix‐loop‐helix protein Id2 is expressed differentially and induced by myc in T‐cell lymphomas

The helix‐loop‐helix protein Id2 is expressed differentially and induced by myc in T‐cell lymphomas

Regulation of Id2 expression by CCAAT/enhancer binding protein

Transcription Factor Networks Directing the Development, Function, and Evolution of Innate Lymphoid Effectors

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