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rdf:type |
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lifeskim:mentions |
umls-concept:C0004561,
umls-concept:C0023434,
umls-concept:C0030705,
umls-concept:C0162638,
umls-concept:C0205178,
umls-concept:C0282637,
umls-concept:C0683598,
umls-concept:C1332421,
umls-concept:C1332710,
umls-concept:C1413191,
umls-concept:C1413206,
umls-concept:C1422341,
umls-concept:C1879547,
umls-concept:C1880177
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pubmed:issue |
4
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pubmed:dateCreated |
2005-10-17
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pubmed:abstractText |
We investigated CD19+CD34+ and CD19+CD34- B cells from cord blood (CB) and typical patients with B cell lineage acute and chronic lymphocytic leukemia (B-ALL and B-CLL) in terms of expression and functions of CXCR5/CXCL13 and CCR7/CCL19. CXCR5 and CCR7 were selectively frequent expressed on B-ALL, B-CLL and CB CD19+CD34+ B cells, but not on CD19+CD34- B cells. Instead of induction of impressive chemotactic responsiveness, CXCL13 and CCL19 together induced significant resistance to TNF-alpha-mediated apoptosis in B-ALL and B-CLL but not CB CD19+CD34+ B cells. B-ALL and B-CLL CD19+CD34+ B cells expressed elevated level of Paternally Expressed Gene 10 (PEG10), and CXCL13 and CCL19 together significantly up-regulated PEG10 expression in the cells. We found that CXCL13 and CCL19 together by means of activation of CXCR5 and CCR7 up-regulated PEG10 expression and function, subsequent stabilized caspase-3 and caspase-8 in B-ALL and B-CLL CD19+CD34+ B cells, and rescued the cells from TNF-alpha-mediated apoptosis. We suggested that normal lymphocytes, especially naive B and T cells, utilized CXCR5/CXCL13 and CCR7/CCL19 for migration, homing, maturation, and cell homeostasis as well as secondary lymphoid tissues organogenesis. Meanwhile certain malignant cells took advantages of CXCR5/CXCL13 and CCR7/CCL19 for infiltration, resistance to apoptosis, and inappropriate proliferation.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD19,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD34,
http://linkedlifedata.com/resource/pubmed/chemical/CCL19 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/CCR7 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/CXCL13 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/CXCR5 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Caspases,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL19,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CXCL13,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, CC,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, CXC,
http://linkedlifedata.com/resource/pubmed/chemical/PEG10 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CCR7,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CXCR5,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Chemokine,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cytokine
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1672-7681
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pubmed:author |
pubmed-author:BaojunHuangH,
pubmed-author:ChunsongHuH,
pubmed-author:JeiXiongX,
pubmed-author:JinYouxinY,
pubmed-author:JinquanTanT,
pubmed-author:JunyanLiuL,
pubmed-author:KejianZhangZ,
pubmed-author:LEEWW,
pubmed-author:LiQunQ,
pubmed-author:MingzhenYangY,
pubmed-author:QingpingGaoG,
pubmed-author:WuQunQ,
pubmed-author:YangXiX,
pubmed-author:ZhangLinjeiL,
pubmed-author:ZhangQiupingQ,
pubmed-author:ZhiminSunS
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pubmed:issnType |
Print
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pubmed:volume |
1
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
280-94
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pubmed:dateRevised |
2008-5-6
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pubmed:meshHeading |
pubmed-meshheading:16225771-Adult,
pubmed-meshheading:16225771-Aged,
pubmed-meshheading:16225771-Antigens, CD19,
pubmed-meshheading:16225771-Antigens, CD34,
pubmed-meshheading:16225771-Apoptosis,
pubmed-meshheading:16225771-B-Lymphocytes,
pubmed-meshheading:16225771-Caspases,
pubmed-meshheading:16225771-Cell Lineage,
pubmed-meshheading:16225771-Chemokine CCL19,
pubmed-meshheading:16225771-Chemokine CXCL13,
pubmed-meshheading:16225771-Chemokines, CC,
pubmed-meshheading:16225771-Chemokines, CXC,
pubmed-meshheading:16225771-Enzyme Activation,
pubmed-meshheading:16225771-Female,
pubmed-meshheading:16225771-Humans,
pubmed-meshheading:16225771-Leukemia, B-Cell,
pubmed-meshheading:16225771-Leukemia, Lymphocytic, Chronic, B-Cell,
pubmed-meshheading:16225771-Male,
pubmed-meshheading:16225771-Middle Aged,
pubmed-meshheading:16225771-Proteins,
pubmed-meshheading:16225771-Receptors, CCR7,
pubmed-meshheading:16225771-Receptors, CXCR5,
pubmed-meshheading:16225771-Receptors, Chemokine,
pubmed-meshheading:16225771-Receptors, Cytokine
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pubmed:year |
2004
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pubmed:articleTitle |
PEG10 activation by co-stimulation of CXCR5 and CCR7 essentially contributes to resistance to apoptosis in CD19+CD34+ B cells from patients with B cell lineage acute and chronic lymphocytic leukemia.
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pubmed:affiliation |
Department of Immunology, College of Basic Medical Sciences, Anhui Medical University, Hefei 230032, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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