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Article ; Online: IgE regulates T helper cell differentiation through FcgammaRIII mediated dendritic cell cytokine modulation.

Blink, Sarah E / Fu, Yang-Xin

2010 Volume 264, Issue 1, Page(s) 54–60

Abstract: Asthma and allergy are characterized by dysregulation of inflammatory responses toward Th2 responses and high serum levels of IgE. IgE plays a role in the effector phase by triggering the degranulation of mast cells after antigen-crosslinking but its ... ...

Abstract	Asthma and allergy are characterized by dysregulation of inflammatory responses toward Th2 responses and high serum levels of IgE. IgE plays a role in the effector phase by triggering the degranulation of mast cells after antigen-crosslinking but its role in the induction of helper T cell differentiation is unknown. We have previously shown lymphotoxin is required for maintaining physiological levels of serum IgE which minimize spontaneous Th1-mediated airway inflammation, suggesting a physiological role for IgE in the regulation of T helper cell differentiation. We describe the mechanism in which IgE modulates inflammation by regulating dendritic cell cytokine production. Physiological levels of IgE suppress IL-12 production in the spleen and lung, suggesting IgE limits Th1 responses in vivo. IgE directly stimulates dendritic cells through FcgammaRIII to suppress IL-12 in vitro and influences APC to skew CD4+ T cells toward Th2 differentiation. We demonstrate a novel role for IgE in regulating differentiation of adaptive inflammatory responses through direct interaction with FcgammaRIII on dendritic cells.
MeSH term(s)	Animals ; Cell Differentiation ; Cells, Cultured ; Cytokines/genetics ; Cytokines/metabolism ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Dendritic Cells/pathology ; Homeodomain Proteins/genetics ; Immunoglobulin E/blood ; Immunoglobulin E/genetics ; Immunoglobulin E/metabolism ; Lung/metabolism ; Lymphotoxin-alpha/genetics ; Lymphotoxin-beta/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Receptor Aggregation ; Receptors, IgG/genetics ; Receptors, IgG/immunology ; Receptors, IgG/metabolism ; Spleen/metabolism ; Th1 Cells/immunology ; Th1 Cells/metabolism ; Th1 Cells/pathology ; Th2 Cells/immunology ; Th2 Cells/metabolism ; Th2 Cells/pathology
Chemical Substances	Cytokines ; Fcgr3 protein, mouse ; Homeodomain Proteins ; Lymphotoxin-alpha ; Lymphotoxin-beta ; Receptors, IgG ; RAG-1 protein (128559-51-3) ; Immunoglobulin E (37341-29-0)
Language	English
Publishing date	2010-05-04
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	80094-6
ISSN	1090-2163 ; 0008-8749
ISSN (online)	1090-2163
ISSN	0008-8749
DOI	10.1016/j.cellimm.2010.04.011
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Zs.A 417: Show issues

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Article: The contribution of gammadelta T cells to the pathogenesis of EAE and MS.

Blink, Sarah E / Miller, Stephen D

Current molecular medicine

2009 Volume 9, Issue 1, Page(s) 15–22

Abstract: Gammadelta T cells are a multifaceted group of cells which have both innate and adaptive characteristics and functions. Although they are most commonly known for their response to mycobacterium and their locations at mucosal sites, their roles in ... ...

Abstract	Gammadelta T cells are a multifaceted group of cells which have both innate and adaptive characteristics and functions. Although they are most commonly known for their response to mycobacterium and their locations at mucosal sites, their roles in autoimmunity are still unclear. gammadelta T cells have been seen in the CSF and lesions of Multiple Sclerosis patients and although their function is not entirely understood, it is clear these cells may have roles in regulating autoimmune inflammation in the CNS. Recent studies have focused on the role of gammadelta T cells in MS and EAE as both pathogenic and protective, their functions within the CNS, the types of subsets and a possible role in Th17 inflammation. In this review we will examine the data acquired from both human patients and the murine models of MS, experimental autoimmune encephalomyelitis (EAE), in order to gain a clear picture of how gammadelta T cells influence pathogenesis of EAE and MS.
MeSH term(s)	Animals ; Arthritis, Experimental/etiology ; Arthritis, Experimental/immunology ; Autoimmunity/immunology ; Central Nervous System/immunology ; Chemotaxis/immunology ; Encephalomyelitis, Autoimmune, Experimental/etiology ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Humans ; Immunity, Active ; Immunity, Innate ; Inflammation/immunology ; Interleukin-17/immunology ; Mice ; Multiple Sclerosis/etiology ; Multiple Sclerosis/immunology ; Neutrophil Infiltration/immunology ; Receptors, Antigen, T-Cell, gamma-delta/immunology ; T-Lymphocyte Subsets/physiology ; T-Lymphocytes/physiology
Chemical Substances	Interleukin-17 ; Receptors, Antigen, T-Cell, gamma-delta
Language	English
Publishing date	2009-02-08
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2064873-X
ISSN	1566-5240
ISSN	1566-5240
DOI	10.2174/156652409787314516
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Article ; Online: γδ T cell subsets play opposing roles in regulating experimental autoimmune encephalomyelitis.

Blink, Sarah E / Caldis, Matthew W / Goings, Gwendolyn E / Harp, Christopher T / Malissen, Bernard / Prinz, Immo / Xu, Dan / Miller, Stephen D

Cellular immunology

2014 Volume 290, Issue 1, Page(s) 39–51

Abstract: γδ T cells are resident in cerebrospinal fluid and central nervous system (CNS) lesions of multiple sclerosis (MS) patients, but as multifaceted cells exhibiting innate and adaptive characteristics, their function remains unknown. Previous studies in ... ...

Abstract	γδ T cells are resident in cerebrospinal fluid and central nervous system (CNS) lesions of multiple sclerosis (MS) patients, but as multifaceted cells exhibiting innate and adaptive characteristics, their function remains unknown. Previous studies in experimental autoimmune encephalomyelitis (EAE) are contradictory and identified these cells as either promoting or suppressing disease pathogenesis. This study examines distinct γδ T cell subsets during EAE and indicates they mediate differential functions in CNS inflammation and demyelination resulting in pathogenesis or protection. We identified two γδ subsets in the CNS, Vγ1(+) and Vγ4(+), with distinct cytokine profiles and tissue specificity. Anti-γδ T cell receptor (TCR) monoclonal antibody (mAb) administration results in activation and downregulation of surface TCR, rendering the cells undetectable, but with opposing effects: anti-Vγ4 treatment exacerbates disease whereas anti-Vγ1 treatment is protective. The Vγ4(+) subset produces multiple pro-inflammatory cytokines including high levels of IL-17, and accounts for 15-20% of the interleukin-17 (IL-17) producing cells in the CNS, but utilize a variant transcriptional program than CD4(+) Th17 cells. In contrast, the Vγ1 subset produces CCR5 ligands, which may promote regulatory T cell differentiation. γδ T cell subsets thus play distinct and opposing roles during EAE, providing an explanation for previous reports and suggesting selective targeting to optimize regulation as a potential therapy for MS.
MeSH term(s)	Animals ; Antibodies, Monoclonal/administration & dosage ; Antibodies, Monoclonal/immunology ; Antibodies, Monoclonal/pharmacology ; Cell Differentiation/immunology ; Central Nervous System/cytology ; Central Nervous System/immunology ; Central Nervous System/pathology ; Down-Regulation ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Female ; Interleukin-17/biosynthesis ; Interleukin-17/immunology ; Lymphocyte Activation/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Multiple Sclerosis/immunology ; Oligodendroglia/immunology ; Receptors, Antigen, T-Cell, gamma-delta/immunology ; Receptors, CCR5/biosynthesis ; Th17 Cells/immunology
Chemical Substances	Antibodies, Monoclonal ; Interleukin-17 ; Receptors, Antigen, T-Cell, gamma-delta ; Receptors, CCR5
Language	English
Publishing date	2014-05-10
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80094-6
ISSN	1090-2163 ; 0008-8749
ISSN (online)	1090-2163
ISSN	0008-8749
DOI	10.1016/j.cellimm.2014.04.013
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Article: Regulation of follicular dendritic cell networks by activated T cells: the role of CD137 signaling.

Sun, Yonglian / Blink, Sarah E / Chen, Jonathan H / Fu, Yang-Xin

Journal of immunology (Baltimore, Md. : 1950)

2005 Volume 175, Issue 2, Page(s) 884–890

Abstract: B cells, but not T cells, are considered to be important for the formation of follicular dendritic cell (FDC) clusters. Stimulation with agonist mAbs against CD137 (4-1BB), a TNFR family member primarily expressed on activated T cells, was effective in ... ...

Abstract	B cells, but not T cells, are considered to be important for the formation of follicular dendritic cell (FDC) clusters. Stimulation with agonist mAbs against CD137 (4-1BB), a TNFR family member primarily expressed on activated T cells, was effective in promoting T cell responses, but paradoxically suppressed T-dependent humoral immunity and autoantibody production in autoimmune disease models. Our present study shows that agonistic anti-CD137 treatment activates T cells, resulting in diminished FDC networks in B cell follicles, which are important components in T-dependent humoral immune responses both before and after the initiation of an immune response. Pretreatment with anti-CD137 before the secondary immunization inhibited memory Ab responses. Interestingly, CD137 costimulation-induced diminishment of FDC is T cell dependent. In addition, both CD4(+) and CD8(+) T cells are recruited into FDC area and are able to regulate FDCs by CD137 costimulation through a direct or indirect mechanism. These studies have revealed a previously unappreciated role of T cells in the regulation of FDC networks.
MeSH term(s)	Adoptive Transfer ; Animals ; Antibodies, Monoclonal/administration & dosage ; Antigens, CD/immunology ; Antigens, CD/metabolism ; Antigens, CD/physiology ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/metabolism ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/metabolism ; Cell Differentiation/genetics ; Cell Differentiation/immunology ; Dendritic Cells, Follicular/cytology ; Dendritic Cells, Follicular/immunology ; Dendritic Cells, Follicular/metabolism ; Down-Regulation/immunology ; Germinal Center/cytology ; Germinal Center/immunology ; Germinal Center/pathology ; Growth Inhibitors/immunology ; Growth Inhibitors/metabolism ; Growth Inhibitors/physiology ; Immunization, Secondary ; Immunoglobulin G/metabolism ; Immunologic Memory/genetics ; Lymphocyte Activation/genetics ; Lymphocyte Activation/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, SCID ; Mice, Transgenic ; Receptors, Antigen, T-Cell, alpha-beta/deficiency ; Receptors, Antigen, T-Cell, alpha-beta/genetics ; Receptors, Nerve Growth Factor/antagonists & inhibitors ; Receptors, Nerve Growth Factor/immunology ; Receptors, Nerve Growth Factor/metabolism ; Receptors, Nerve Growth Factor/physiology ; Receptors, Tumor Necrosis Factor/antagonists & inhibitors ; Receptors, Tumor Necrosis Factor/immunology ; Receptors, Tumor Necrosis Factor/metabolism ; Receptors, Tumor Necrosis Factor/physiology ; Signal Transduction/genetics ; Signal Transduction/immunology ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism ; T-Lymphocyte Subsets/transplantation ; Tumor Necrosis Factor Receptor Superfamily, Member 9
Chemical Substances	Antibodies, Monoclonal ; Antigens, CD ; Growth Inhibitors ; Immunoglobulin G ; Receptors, Antigen, T-Cell, alpha-beta ; Receptors, Nerve Growth Factor ; Receptors, Tumor Necrosis Factor ; Tnfrsf9 protein, mouse ; Tumor Necrosis Factor Receptor Superfamily, Member 9
Language	English
Publishing date	2005-06-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S.
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.175.2.884
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Article: Inhibition of Th2-mediated allergic airway inflammatory disease by CD137 costimulation.

Sun, Yonglian / Blink, Sarah E / Liu, Wenhua / Lee, Youjin / Chen, Bohao / Solway, Julian / Weinstock, Joel / Chen, Lieping / Fu, Yang-Xin

Journal of immunology (Baltimore, Md. : 1950)

2006 Volume 177, Issue 2, Page(s) 814–821

Abstract: The engagement of CD137 (4-1BB), an inducible T cell costimulatory receptor and member of the TNF receptor superfamily, by agonistic Abs can promote strong tumor and viral immunity mediated by CD8(+) T cells and stimulate IFN-gamma production. However, ... ...

Abstract	The engagement of CD137 (4-1BB), an inducible T cell costimulatory receptor and member of the TNF receptor superfamily, by agonistic Abs can promote strong tumor and viral immunity mediated by CD8(+) T cells and stimulate IFN-gamma production. However, its role in Th2-mediated immune responses has not been well defined. To address this issue, we studied the function of CD137 engagement using an allergic airway disease model in which the mice were sensitized with inactivated Schistosoma mansoni eggs followed by S. mansoni egg Ag challenge directly in the airways and Th1/2 cytokine production was monitored. Interestingly, treatment of C57BL/6 mice with agonistic anti-CD137 (2A) during sensitization completely prevents allergic airway inflammation, as shown by a clear inhibition of T cell and eosinophil infiltration into the lung tissue and airways, accompanied by diminished Th2 cytokine production and reduced serum IgE levels, as well as a reduction of airway hyperresponsiveness. At various time points after immunization, restimulated splenocytes from 2A-treated mice displayed reduced proliferation and Th2 cytokine production. In accordance with this, agonistic Ab to CD137 can directly coinhibit Th2 responses in vitro although it costimulates Th1 responses. CD137-mediated suppression of Th2 response is independent of IFN-gamma and T regulatory cells. Our study has identified a novel pathway to inhibit Th2 responses in a CD137-dependent fashion.
MeSH term(s)	Animals ; Antibodies, Monoclonal/administration & dosage ; Antigens, CD/immunology ; Antigens, CD/physiology ; Antigens, Helminth/administration & dosage ; Bronchial Hyperreactivity/immunology ; Bronchial Hyperreactivity/pathology ; Bronchial Hyperreactivity/prevention & control ; Bronchoalveolar Lavage Fluid/immunology ; Cells, Cultured ; Down-Regulation/immunology ; Female ; GATA3 Transcription Factor/antagonists & inhibitors ; GATA3 Transcription Factor/biosynthesis ; GATA3 Transcription Factor/genetics ; Immunoglobulin E/biosynthesis ; Interferon-gamma/physiology ; Lung/immunology ; Lung/metabolism ; Lymphocyte Activation/immunology ; Mice ; Mice, Inbred C57BL ; Receptors, Nerve Growth Factor/agonists ; Receptors, Nerve Growth Factor/immunology ; Receptors, Nerve Growth Factor/physiology ; Receptors, Tumor Necrosis Factor/agonists ; Receptors, Tumor Necrosis Factor/immunology ; Receptors, Tumor Necrosis Factor/physiology ; Schistosoma mansoni/immunology ; Schistosomiasis/immunology ; Schistosomiasis/pathology ; Schistosomiasis/prevention & control ; Signal Transduction/immunology ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism ; Th2 Cells/immunology ; Th2 Cells/metabolism ; Tumor Necrosis Factor Receptor Superfamily, Member 9
Chemical Substances	Antibodies, Monoclonal ; Antigens, CD ; Antigens, Helminth ; GATA3 Transcription Factor ; Gata3 protein, mouse ; Receptors, Nerve Growth Factor ; Receptors, Tumor Necrosis Factor ; Tnfrsf9 protein, mouse ; Tumor Necrosis Factor Receptor Superfamily, Member 9 ; Immunoglobulin E (37341-29-0) ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2006-06-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
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.177.2.814
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Article: Lymphotoxin is required for maintaining physiological levels of serum IgE that minimizes Th1-mediated airway inflammation.

Kang, Hyung-Sik / Blink, Sarah E / Chin, Robert K / Lee, Youjin / Kim, Oliver / Weinstock, Joel / Waldschmidt, Thomas / Conrad, Daniel / Chen, Bohao / Solway, Julian / Sperling, Anne I / Fu, Yang-Xin

The Journal of experimental medicine

2003 Volume 198, Issue 11, Page(s) 1643–1652

Abstract: ... infiltration by activated T helper (Th) 2 cells, the physiological role of immunoglobulin E (IgE) in the airway ...

Abstract	Although elevated levels of IgE in asthmatic patients are strongly associated with lung infiltration by activated T helper (Th) 2 cells, the physiological role of immunoglobulin E (IgE) in the airway remains largely undefined. Lymphotoxin-deficient alpha (LTalpha-/-) mice exhibit increased airway inflammation, paradoxically accompanied by diminished levels of IgE and reduced airway hyperresponsiveness in response to both environmental and induced antigen challenge. The severe lung inflammation in LTalpha-/- mice is Th1 in nature and can be alleviated by IgE reconstitution. Conversely, depletion of IgE in wild-type mice recapitulates the lung pathologies of LTalpha-/- mice. Therefore, this work has revealed that lymphotoxin is essential for IgE production, and a physiological role of IgE in the airway may consist of maintaining the balance of Th1 and Th2 responses to prevent aberrant inflammation.
MeSH term(s)	Animals ; Bronchial Hyperreactivity/immunology ; Bronchoalveolar Lavage Fluid ; Enzyme-Linked Immunosorbent Assay ; Flow Cytometry ; Immunoglobulin E/blood ; Immunoglobulin E/deficiency ; Lymphotoxin-alpha/genetics ; Lymphotoxin-alpha/physiology ; Mice ; Mice, Knockout ; Respiratory Mechanics ; Th1 Cells/immunology
Chemical Substances	Lymphotoxin-alpha ; Immunoglobulin E (37341-29-0)
Language	English
Publishing date	2003-12-01
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20021784
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Ua VI Zs.107: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article: Lymphotoxin pathway directs thymic Aire expression.

Chin, Robert K / Lo, James C / Kim, Oliver / Blink, Sarah E / Christiansen, Peter A / Peterson, Pärt / Wang, Yang / Ware, Carl / Fu, Yang-Xin

Nature immunology

2003 Volume 4, Issue 11, Page(s) 1121–1127

Abstract: The autoimmune regulator Aire is a key mediator of central tolerance for peripherally restricted antigens. Its absence in human patients results in autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy. The cellular signals that regulate Aire ... ...

Abstract	The autoimmune regulator Aire is a key mediator of central tolerance for peripherally restricted antigens. Its absence in human patients results in autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy. The cellular signals that regulate Aire expression are undefined. We show here that lymphotoxin signaling is necessary for the expression of Aire and its downstream target genes. The failure of Aire induction in the thymi of lymphotoxin-deficient and lymphotoxin-beta receptor-deficient mice contributes to overt autoimmunity against self antigens normally protected by Aire. Conversely, stimulation of lymphotoxin-beta receptor by agonistic antibody leads to increased expression of Aire and tissue-restricted antigens in both intact thymi and cultured thymic epithelial cell line. These findings define the essential cross-talk between thymocytes and thymic stroma that is required for central tolerance.
MeSH term(s)	Animals ; Autoantibodies/immunology ; Immune Tolerance/immunology ; Insulin/immunology ; Lymphotoxin beta Receptor ; Lymphotoxin-alpha/genetics ; Lymphotoxin-alpha/metabolism ; Mice ; Receptors, Tumor Necrosis Factor/genetics ; Receptors, Tumor Necrosis Factor/metabolism ; Signal Transduction/physiology ; Spleen/cytology ; Spleen/transplantation ; Thymus Gland/metabolism ; Transcription Factors/biosynthesis ; Transcription Factors/genetics ; AIRE Protein
Chemical Substances	Autoantibodies ; Insulin ; LTBR protein, human ; Ltbr protein, mouse ; Lymphotoxin beta Receptor ; Lymphotoxin-alpha ; Receptors, Tumor Necrosis Factor ; Transcription Factors
Language	English
Publishing date	2003-09-28
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/ni982
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Article: Specificities of N-acetylglucosamine-6-O-sulfotransferases in relation to L-selectin ligand synthesis and tumor-associated enzyme expression.

Uchimura, Kenji / El-Fasakhany, Fathy M / Hori, Mayuko / Hemmerich, Stefan / Blink, Sarah E / Kansas, Geoffrey S / Kanamori, Akiko / Kumamoto, Kensuke / Kannagi, Reiji / Muramatsu, Takashi

The Journal of biological chemistry

2001 Volume 277, Issue 6, Page(s) 3979–3984

Abstract: N-Acetylglucosamine-6-O-sulfotransferase (GlcNAc6ST) catalyzes the transfer of sulfate from adenosine 3'-phosphate,5'-phosphosulfate to the C-6 position of the non-reducing GlcNAc. Three human GlcNAc6STs, namely GlcNAc6ST-1, GlcNAc6ST-2 (HEC-GlcNAc6ST), ... ...

Abstract	N-Acetylglucosamine-6-O-sulfotransferase (GlcNAc6ST) catalyzes the transfer of sulfate from adenosine 3'-phosphate,5'-phosphosulfate to the C-6 position of the non-reducing GlcNAc. Three human GlcNAc6STs, namely GlcNAc6ST-1, GlcNAc6ST-2 (HEC-GlcNAc6ST), and GlcNAc6ST-3 (I-GlcNAc6ST), were produced as fusion proteins to protein A, and their substrate specificities as well as their enzymological properties were determined. Both GlcNAc6ST-1 and GlcNAc6ST-2 efficiently utilized the following oligosaccharide structures as acceptors: GlcNAcbeta1-6[Galbeta1-3]GalNAc-pNP (core 2), GlcNAcbeta1-6ManOMe, and GlcNAcbeta1-2Man. The ratios of activities to these substrates were not significantly different between the two enzymes. However, GlcNAc6ST-2 but not GlcNAc6ST-1 acted on core 3 of GlcNAcbeta1-3GalNAc-pNP. GlcNAc6ST-3 used only the core 2 structure among the above mentioned oligosaccharide structures. The ability of GlcNAc6ST-1 to sulfate core 2 structure as efficiently as GlcNAc6ST-2 is consistent with the view that GlcNAc6ST-1 is also involved in the synthesis of l-selectin ligand. Indeed, cells doubly transfected with GlcNAc6ST-1 and fucosyltransferase VII cDNAs supported the rolling of L-selectin-expressing cells. The activity of GlcNAc6ST-2 on core 3 and its expression in mucinous adenocarcinoma suggested that this enzyme corresponds to the sulfotransferase, which is specifically expressed in mucinous adenocarcinoma (Seko, A., Sumiya, J., Yonezawa, S., Nagata, K., and Yamashita, K. (2000) Glycobiology 10, 919-929).
MeSH term(s)	Base Sequence ; Colonic Neoplasms/enzymology ; Colonic Neoplasms/pathology ; DNA Primers ; Humans ; Isoenzymes/metabolism ; L-Selectin/metabolism ; Oligosaccharides/chemistry ; Oligosaccharides/metabolism ; Substrate Specificity ; Sulfotransferases/genetics ; Sulfotransferases/metabolism ; Transfection ; Carbohydrate Sulfotransferases
Chemical Substances	DNA Primers ; Isoenzymes ; Oligosaccharides ; L-Selectin (126880-86-2) ; Sulfotransferases (EC 2.8.2.-)
Language	English
Publishing date	2001-11-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M106587200
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