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Article ; Online: TSLP shapes the pathogenic responses of memory CD4

Rochman, Yrina / Kotliar, Michael / Ben-Baruch Morgenstern, Netali / Barski, Artem / Wen, Ting / Rothenberg, Marc E

2023 Volume 16, Issue 802, Page(s) eadg6360

Abstract: The cytokine thymic stromal lymphopoietin (TSLP) mediates type 2 immune responses, and treatments that interfere with TSLP activity are in clinical use for asthma. Here, we investigated whether TSLP contributes to allergic inflammation by directly ... ...

Abstract	The cytokine thymic stromal lymphopoietin (TSLP) mediates type 2 immune responses, and treatments that interfere with TSLP activity are in clinical use for asthma. Here, we investigated whether TSLP contributes to allergic inflammation by directly stimulating human CD4
MeSH term(s)	Humans ; CD4-Positive T-Lymphocytes ; Cytokines ; Eosinophilic Esophagitis ; STAT5 Transcription Factor/genetics ; T-Lymphocytes ; Thymic Stromal Lymphopoietin
Chemical Substances	Cytokines ; STAT5 Transcription Factor ; Thymic Stromal Lymphopoietin (GT0IL38SP4)
Language	English
Publishing date	2023-09-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2417226-1
ISSN	1937-9145 ; 1945-0877
ISSN (online)	1937-9145
ISSN	1945-0877
DOI	10.1126/scisignal.adg6360
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The minichromosome maintenance complex drives esophageal basal zone hyperplasia.

Rochman, Mark / Rochman, Yrina / Caldwell, Julie M / Mack, Lydia E / Besse, John A / Manes, Nathan P / Yoon, Sung Hwan / Shoda, Tetsuo / Nita-Lazar, Aleksandra / Rothenberg, Marc E

JCI insight

2023 Volume 8, Issue 17

Abstract: Eosinophilic esophagitis (EoE) is a chronic gastrointestinal disorder characterized by food antigen-driven eosinophilic inflammation and hyperproliferation of esophageal mucosa. By utilizing a large-scale, proteomic screen of esophageal biopsies, we ... ...

Abstract	Eosinophilic esophagitis (EoE) is a chronic gastrointestinal disorder characterized by food antigen-driven eosinophilic inflammation and hyperproliferation of esophageal mucosa. By utilizing a large-scale, proteomic screen of esophageal biopsies, we aimed to uncover molecular drivers of the disease. Proteomic analysis by liquid chromatography-tandem mass spectrometry identified 402 differentially expressed proteins (DEPs) that correlated with the EoE transcriptome. Immune cell-related proteins were among the most highly upregulated DEPs in EoE compared with controls, whereas proteins linked to epithelial differentiation were primarily downregulated. Notably, in the inflamed esophageal tissue, all 6 subunits of the minichromosome maintenance (MCM) complex, a DNA helicase essential for genomic DNA replication, were significantly upregulated at the gene and protein levels. Furthermore, treating esophageal epithelial cells with a known inhibitor of the MCM complex (ciprofloxacin) blocked esophageal epithelial proliferation. In a murine model of EoE driven by overexpression of IL-13, ciprofloxacin treatment decreased basal zone thickness and reduced dilated intercellular spaces by blocking the transition of epithelial cells through the S-phase of the cell cycle. Collectively, a broad-spectrum proteomic screen has identified the involvement of the MCM complex in EoE and has highlighted MCM inhibitors as potential therapeutic agents for the disease.
MeSH term(s)	Humans ; Animals ; Mice ; Hyperplasia/pathology ; Proteomics ; Eosinophilic Esophagitis ; Epithelial Cells/metabolism
Language	English
Publishing date	2023-09-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.172143
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Article ; Online: The minichromosome maintenance complex drives esophageal basal zone hyperplasia

Mark Rochman / Yrina Rochman / Julie M. Caldwell / Lydia E. Mack / John A. Besse / Nathan P. Manes / Sung Hwan Yoon / Tetsuo Shoda / Aleksandra Nita-Lazar / Marc E. Rothenberg

JCI Insight, Vol 8, Iss

2023 Volume 17

Abstract: Eosinophilic esophagitis (EoE) is a chronic gastrointestinal disorder characterized by food antigen–driven eosinophilic inflammation and hyperproliferation of esophageal mucosa. By utilizing a large-scale, proteomic screen of esophageal biopsies, we ... ...

Abstract	Eosinophilic esophagitis (EoE) is a chronic gastrointestinal disorder characterized by food antigen–driven eosinophilic inflammation and hyperproliferation of esophageal mucosa. By utilizing a large-scale, proteomic screen of esophageal biopsies, we aimed to uncover molecular drivers of the disease. Proteomic analysis by liquid chromatography–tandem mass spectrometry identified 402 differentially expressed proteins (DEPs) that correlated with the EoE transcriptome. Immune cell–related proteins were among the most highly upregulated DEPs in EoE compared with controls, whereas proteins linked to epithelial differentiation were primarily downregulated. Notably, in the inflamed esophageal tissue, all 6 subunits of the minichromosome maintenance (MCM) complex, a DNA helicase essential for genomic DNA replication, were significantly upregulated at the gene and protein levels. Furthermore, treating esophageal epithelial cells with a known inhibitor of the MCM complex (ciprofloxacin) blocked esophageal epithelial proliferation. In a murine model of EoE driven by overexpression of IL-13, ciprofloxacin treatment decreased basal zone thickness and reduced dilated intercellular spaces by blocking the transition of epithelial cells through the S-phase of the cell cycle. Collectively, a broad-spectrum proteomic screen has identified the involvement of the MCM complex in EoE and has highlighted MCM inhibitors as potential therapeutic agents for the disease.
Keywords	Gastroenterology ; Immunology ; Medicine ; R
Subject code	570
Language	English
Publishing date	2023-09-01T00:00:00Z
Publisher	American Society for Clinical investigation
Document type	Article ; Online
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Article ; Online: Local type 2 immunity in eosinophilic gastritis.

Ben-Baruch Morgenstern, Netali / Shoda, Tetsuo / Rochman, Yrina / Caldwell, Julie M / Collins, Margaret H / Mukkada, Vincent / Putnam, Philip E / Bolton, Scott M / Felton, Jennifer M / Rochman, Mark / Murray-Petzold, Cristin / Kliewer, Kara L / Rothenberg, Marc E

The Journal of allergy and clinical immunology

2023 Volume 152, Issue 1, Page(s) 136–144

Abstract: Background: Eosinophilic gastritis (EoG) associates with type 2 immunity. However, the type 2 cytokine cellular source, gastric T-cell composition, and gastric T-cell relationship (or relationships) with disease pathology remain understudied.: ... ...

Abstract	Background: Eosinophilic gastritis (EoG) associates with type 2 immunity. However, the type 2 cytokine cellular source, gastric T-cell composition, and gastric T-cell relationship (or relationships) with disease pathology remain understudied. Objective: We defined gastric T-cell populations and their association with histologic and endoscopic EoG pathology. Methods: Gastric biopsy samples (n = 6 EoG, n = 7 control) were subjected to histologic, endoscopic, and flow cytometry analyses. In a complementary cohort (n = 83 EoG), IL4, IL5, and IL13 mRNA levels were correlated with EoG pathologic parameters. Results: Gastric biopsy samples contained CD3 Conclusions: EoG is a T
MeSH term(s)	Humans ; Interleukin-13 ; Interleukin-4 ; Interleukin-5 ; Cytokines ; RNA, Messenger
Chemical Substances	Interleukin-13 ; Interleukin-4 (207137-56-2) ; Interleukin-5 ; Cytokines ; RNA, Messenger
Language	English
Publishing date	2023-02-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2023.01.021
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Article ; Online: Environmental allergens trigger type 2 inflammation through ripoptosome activation.

Brusilovsky, Michael / Rochman, Mark / Rochman, Yrina / Caldwell, Julie M / Mack, Lydia E / Felton, Jennifer M / Habel, Jeff E / Porollo, Aleksey / Pasare, Chandrashekhar / Rothenberg, Marc E

Nature immunology

2021 Volume 22, Issue 10, Page(s) 1316–1326

Abstract: Environmental allergens, including fungi, insects and mites, trigger type 2 immunity; however, the innate sensing mechanisms and initial signaling events remain unclear. Herein, we demonstrate that allergens trigger RIPK1-caspase 8 ripoptosome activation ...

Abstract	Environmental allergens, including fungi, insects and mites, trigger type 2 immunity; however, the innate sensing mechanisms and initial signaling events remain unclear. Herein, we demonstrate that allergens trigger RIPK1-caspase 8 ripoptosome activation in epithelial cells. The active caspase 8 subsequently engages caspases 3 and 7, which directly mediate intracellular maturation and release of IL-33, a pro-atopy, innate immunity, alarmin cytokine. Mature IL-33 maintained functional interaction with the cognate ST2 receptor and elicited potent pro-atopy inflammatory activity in vitro and in vivo. Inhibiting caspase 8 pharmacologically and deleting murine Il33 and Casp8 each attenuated allergic inflammation in vivo. Clinical data substantiated ripoptosome activation and IL-33 maturation as likely contributors to human allergic inflammation. Our findings reveal an epithelial barrier, allergen-sensing mechanism that converges on the ripoptosome as an intracellular molecular signaling platform, triggering type 2 innate immune responses. These findings have significant implications for understanding and treating human allergic diseases.
MeSH term(s)	Adolescent ; Allergens/immunology ; Animals ; Caspase 8/immunology ; Cell Line ; Cell Line, Tumor ; Child ; Child, Preschool ; Cytokines/immunology ; Epithelial Cells/immunology ; Female ; HEK293 Cells ; Humans ; Hypersensitivity/immunology ; Immunity, Innate/immunology ; Inflammation/immunology ; Interleukin-33/immunology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Signal Transduction/immunology
Chemical Substances	Allergens ; Cytokines ; Interleukin-33 ; Caspase 8 (EC 3.4.22.-)
Language	English
Publishing date	2021-09-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/s41590-021-01011-2
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Zs.A 5294: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Functional characterization of human T cell hyporesponsiveness induced by CTLA4-Ig.

Rochman, Yrina / Yukawa, Masashi / Kartashov, Andrey V / Barski, Artem

PloS one

2015 Volume 10, Issue 4, Page(s) e0122198

Abstract: During activation, T cells integrate multiple signals from APCs and cytokine milieu. The blockade of these signals can have clinical benefits as exemplified by CTLA4-Ig, which blocks interaction of B7 co-stimulatory molecules on APCs with CD28 on T cells. ...

Abstract	During activation, T cells integrate multiple signals from APCs and cytokine milieu. The blockade of these signals can have clinical benefits as exemplified by CTLA4-Ig, which blocks interaction of B7 co-stimulatory molecules on APCs with CD28 on T cells. Variants of CTLA4-Ig, abatacept and belatacept are FDA approved as immunosuppressive agents in arthritis and transplantation, yet murine studies suggested that CTLA4-Ig could be beneficial in a number of other diseases. However, detailed analysis of human CD4 cell hyporesponsivness induced by CTLA4-Ig has not been performed. Herein, we established a model to study the effect of CTLA4-Ig on the activation of human naïve T cells in a human mixed lymphocytes system. Comparison of human CD4 cells activated in the presence or absence of CTLA4-Ig showed that co-stimulation blockade during TCR activation does not affect NFAT signaling but results in decreased activation of NF-κB and AP-1 transcription factors followed by a profound decrease in proliferation and cytokine production. The resulting T cells become hyporesponsive to secondary activation and, although capable of receiving TCR signals, fail to proliferate or produce cytokines, demonstrating properties of anergic cells. However, unlike some models of T cell anergy, these cells did not possess increased levels of the TCR signaling inhibitor CBLB. Rather, the CTLA4-Ig-induced hyporesponsiveness was associated with an elevated level of p27kip1 cyclin-dependent kinase inhibitor.
MeSH term(s)	Antigens, Surface/genetics ; Antigens, Surface/metabolism ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/metabolism ; CTLA-4 Antigen/genetics ; CTLA-4 Antigen/immunology ; Clonal Anergy ; Cyclin-Dependent Kinase Inhibitor p27/metabolism ; Cytokines/biosynthesis ; Gene Expression ; Gene Expression Profiling ; Humans ; Immunoglobulins/genetics ; Immunoglobulins/immunology ; Immunologic Memory ; Immunophenotyping ; Lymphocyte Activation/drug effects ; Lymphocyte Activation/immunology ; Phenotype ; Receptors, Antigen, T-Cell/metabolism ; Recombinant Fusion Proteins/immunology ; Recombinant Fusion Proteins/pharmacology ; Signal Transduction ; T-Lymphocyte Subsets/drug effects ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism ; T-Lymphocytes/drug effects ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism ; Transcriptome ; Ubiquitin-Protein Ligases/metabolism
Chemical Substances	Antigens, Surface ; CTLA-4 Antigen ; Cytokines ; Immunoglobulins ; Receptors, Antigen, T-Cell ; Recombinant Fusion Proteins ; Cyclin-Dependent Kinase Inhibitor p27 (147604-94-2) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2015-04-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0122198
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Article ; Online: Functional characterization of human T cell hyporesponsiveness induced by CTLA4-Ig.

Yrina Rochman / Masashi Yukawa / Andrey V Kartashov / Artem Barski

PLoS ONE, Vol 10, Iss 4, p e

2015 Volume 0122198

Abstract	During activation, T cells integrate multiple signals from APCs and cytokine milieu. The blockade of these signals can have clinical benefits as exemplified by CTLA4-Ig, which blocks interaction of B7 co-stimulatory molecules on APCs with CD28 on T cells. Variants of CTLA4-Ig, abatacept and belatacept are FDA approved as immunosuppressive agents in arthritis and transplantation, yet murine studies suggested that CTLA4-Ig could be beneficial in a number of other diseases. However, detailed analysis of human CD4 cell hyporesponsivness induced by CTLA4-Ig has not been performed. Herein, we established a model to study the effect of CTLA4-Ig on the activation of human naïve T cells in a human mixed lymphocytes system. Comparison of human CD4 cells activated in the presence or absence of CTLA4-Ig showed that co-stimulation blockade during TCR activation does not affect NFAT signaling but results in decreased activation of NF-κB and AP-1 transcription factors followed by a profound decrease in proliferation and cytokine production. The resulting T cells become hyporesponsive to secondary activation and, although capable of receiving TCR signals, fail to proliferate or produce cytokines, demonstrating properties of anergic cells. However, unlike some models of T cell anergy, these cells did not possess increased levels of the TCR signaling inhibitor CBLB. Rather, the CTLA4-Ig-induced hyporesponsiveness was associated with an elevated level of p27kip1 cyclin-dependent kinase inhibitor.
Keywords	Medicine ; R ; Science ; Q
Subject code	570
Language	English
Publishing date	2015-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Single-cell RNA sequencing identifies inflammatory tissue T cells in eosinophilic esophagitis.

Wen, Ting / Aronow, Bruce J / Rochman, Yrina / Rochman, Mark / Kc, Kiran / Dexheimer, Phil J / Putnam, Philip / Mukkada, Vincent / Foote, Heather / Rehn, Kira / Darko, Sam / Douek, Daniel / Rothenberg, Marc E

The Journal of clinical investigation

2019 Volume 129, Issue 5, Page(s) 2014–2028

Abstract: T cell heterogeneity is highly relevant to allergic disorders. We resolved the heterogeneity of human tissue CD3+ T cells during allergic inflammation, focusing on a tissue-specific allergic disease, eosinophilic esophagitis (EoE). We investigated 1088 ... ...

Abstract	T cell heterogeneity is highly relevant to allergic disorders. We resolved the heterogeneity of human tissue CD3+ T cells during allergic inflammation, focusing on a tissue-specific allergic disease, eosinophilic esophagitis (EoE). We investigated 1088 single T cells derived from patients with a spectrum of disease activity. Eight disparate tissue T cell subtypes (designated T1-T8) were identified, with T7 and T8 enriched in the diseased tissue. The phenotypes of T7 and T8 resemble putative Treg (FOXP3+) and effector Th2-like (GATA3+) cells, respectively. Prodigious levels of IL-5 and IL-13 were confined to HPGDS+ CRTH2+IL-17RB+FFAR3+CD4+ T8 effector Th2 cells. EoE severity closely paralleled a lipid/fatty acid-induced activation node highlighted by the expression of the short-chain fatty acid receptor FFAR3. Ligands for FFAR3 induced Th2 cytokine production from human and murine T cells, including in an in vivo allergy model. Therefore, we elucidated the defining characteristics of tissue-residing CD3+ T cells in EoE, a specific enrichment of CD4+ Treg and effector Th2 cells, confinement of type 2 cytokine production to the CD4+ effector population, a highly likely role for FFAR3 in amplifying local Th2 responses in EoE, and a resource to further dissect tissue lymphocytes and allergic responses.
MeSH term(s)	Adolescent ; Animals ; Biopsy ; CD3 Complex/analysis ; Cell Separation ; Child ; Child, Preschool ; Computational Biology ; Endoscopy ; Eosinophilic Esophagitis/genetics ; Eosinophilic Esophagitis/immunology ; Female ; Flow Cytometry ; GATA3 Transcription Factor/immunology ; Humans ; Inflammation ; Interleukin-13/immunology ; Interleukin-5/immunology ; Ligands ; Lung/metabolism ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred BALB C ; Phenotype ; Sequence Analysis, RNA/methods ; Single-Cell Analysis/methods ; T-Lymphocytes/immunology ; T-Lymphocytes, Regulatory/immunology ; Th2 Cells/immunology
Chemical Substances	CD3 Complex ; GATA3 Transcription Factor ; GATA3 protein, human ; IL5 protein, human ; Interleukin-13 ; Interleukin-5 ; Ligands
Language	English
Publishing date	2019-04-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI125917
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Article: Thymic stromal lymphopoietin: a new cytokine in asthma.

Rochman, Yrina / Leonard, Warren J

Current opinion in pharmacology

2008 Volume 8, Issue 3, Page(s) 249–254

Abstract: Airway epithelial cells provide mechanical and immune protection against pathogens and allergens. Following activation, these cells produce a wide range of cytokines including thymic stromal lymphopoietin (TSLP). Recently it was established that a high ... ...

Abstract	Airway epithelial cells provide mechanical and immune protection against pathogens and allergens. Following activation, these cells produce a wide range of cytokines including thymic stromal lymphopoietin (TSLP). Recently it was established that a high level of TSLP is associated with asthma in mice and in humans. These findings suggest that interfering with the ability of cells to respond to TSLP might prevent the development of airway inflammation. Our review presents current knowledge on mediators that induce TSLP production and on the actions of TSLP on different populations of cells that are related to airway inflammation. TSLP affects dendritic cells, T cells, NKT cells, and mast cells, indicative of the broad role of TSLP in the regulation of inflammatory/allergic processes.
MeSH term(s)	Animals ; Asthma/drug therapy ; Asthma/etiology ; Cytokines/physiology ; Dendritic Cells/physiology ; Humans ; Lymphocytes/physiology ; Mast Cells/physiology ; Receptors, Cytokine/physiology ; Signal Transduction
Chemical Substances	CRLF2 protein, human ; Cytokines ; Receptors, Cytokine ; thymic stromal lymphopoietin (GT0IL38SP4)
Language	English
Publishing date	2008-04-29
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2037057-X
ISSN	1471-4973 ; 1471-4892
ISSN (online)	1471-4973
ISSN	1471-4892
DOI	10.1016/j.coph.2008.03.002
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Article ; Online: The role of thymic stromal lymphopoietin in CD8+ T cell homeostasis.

Rochman, Yrina / Leonard, Warren J

Journal of immunology (Baltimore, Md. : 1950)

2008 Volume 181, Issue 11, Page(s) 7699–7705

Abstract: Thymic stromal lymphopoietin (TSLP) is a cytokine produced by stromal cells, epithelial cells, and basophils that acts on dendritic cells, mast cells, and CD4(+) T cells. The receptor for TSLP contains a TSLP-specific receptor chain (TSLPR) and the IL-7R ...

Abstract	Thymic stromal lymphopoietin (TSLP) is a cytokine produced by stromal cells, epithelial cells, and basophils that acts on dendritic cells, mast cells, and CD4(+) T cells. The receptor for TSLP contains a TSLP-specific receptor chain (TSLPR) and the IL-7R alpha-chain. Although IL-7 critically controls the expansion and survival of naive and memory CD8(+) T cells, an action for TSLP on CD8(+) T cells has not been reported. We now demonstrate that CD8(+) T cells express TSLPR and that TSLP activates both STAT5 and Akt and induces Bcl-2 in these cells. Correspondingly, TSLP increases CD8(+) T cell survival in vitro as well as in wild-type and T-depleted mice in vivo, without altering the homeostatic proliferation of these cells. Moreover, TSLP can maintain CD8(+) T cells even in the absence of IL-7. Thus, our data reveal that TSLP contributes to CD8(+) T cell homeostasis in both normal and lymphopenic conditions.
MeSH term(s)	Animals ; Basophils/immunology ; Basophils/metabolism ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/metabolism ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/metabolism ; Cell Proliferation ; Cell Survival/immunology ; Cytokines/biosynthesis ; Cytokines/genetics ; Cytokines/immunology ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Epithelial Cells/immunology ; Epithelial Cells/metabolism ; Gene Expression Regulation/genetics ; Gene Expression Regulation/immunology ; Homeostasis/genetics ; Homeostasis/immunology ; Immunoglobulins ; Immunologic Memory/genetics ; Immunologic Memory/immunology ; Lymphopenia/genetics ; Lymphopenia/immunology ; Lymphopenia/metabolism ; Mast Cells/immunology ; Mast Cells/metabolism ; Mice ; Mice, Knockout ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/immunology ; Proto-Oncogene Proteins c-akt/metabolism ; Proto-Oncogene Proteins c-bcl-2/genetics ; Proto-Oncogene Proteins c-bcl-2/immunology ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Receptors, Cytokine/genetics ; Receptors, Cytokine/immunology ; Receptors, Cytokine/metabolism ; Receptors, Interleukin-7/biosynthesis ; Receptors, Interleukin-7/genetics ; Receptors, Interleukin-7/immunology ; STAT5 Transcription Factor/genetics ; STAT5 Transcription Factor/immunology ; STAT5 Transcription Factor/metabolism ; Stromal Cells/immunology ; Stromal Cells/metabolism
Chemical Substances	Cytokines ; Immunoglobulins ; Proto-Oncogene Proteins c-bcl-2 ; Receptors, Cytokine ; Receptors, Interleukin-7 ; STAT5 Transcription Factor ; Tslpr protein, mouse ; interleukin-7 receptor, alpha chain ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; thymic stromal lymphopoietin (GT0IL38SP4)
Language	English
Publishing date	2008-11-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.181.11.7699
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