|
|
|
|
LEADER |
01000naa a22002652 4500 |
001 |
NLM186923694 |
003 |
DE-627 |
005 |
20231223175035.0 |
007 |
cr uuu---uuuuu |
008 |
231223s2009 xx |||||o 00| ||eng c |
024 |
7 |
|
|a 10.1016/j.clim.2009.01.015
|2 doi
|
028 |
5 |
2 |
|a pubmed24n0623.xml
|
035 |
|
|
|a (DE-627)NLM186923694
|
035 |
|
|
|a (NLM)19269255
|
040 |
|
|
|a DE-627
|b ger
|c DE-627
|e rakwb
|
041 |
|
|
|a eng
|
100 |
1 |
|
|a Chen, Rong-Fu
|e verfasserin
|4 aut
|
245 |
1 |
0 |
|a Combination of CTLA-4 and TGFbeta1 gene polymorphisms associated with dengue hemorrhagic fever and virus load in a dengue-2 outbreak
|
264 |
|
1 |
|c 2009
|
336 |
|
|
|a Text
|b txt
|2 rdacontent
|
337 |
|
|
|a ƒaComputermedien
|b c
|2 rdamedia
|
338 |
|
|
|a ƒa Online-Ressource
|b cr
|2 rdacarrier
|
500 |
|
|
|a Date Completed 09.06.2009
|
500 |
|
|
|a Date Revised 21.11.2013
|
500 |
|
|
|a published: Print-Electronic
|
500 |
|
|
|a Citation Status MEDLINE
|
520 |
|
|
|a The pathogenesis of dengue hemorrhagic fever (DHF) has been considered to be massive immune activation of T cells. Abnormal expression of the immune regulatory molecules, CTLA-4 and TGFbeta1, leads to disturbances of regulatory T cell immune response. We investigate the contribution of CTLA-4 and TGFbeta1 in DHF by analyzing them for association with virus load in blood and polymorphisms of CTLA-4 +49A/G, and TGFbeta1 -509C/T in a DEN-2 outbreak. The increased frequency of the TGFbeta1 -509 CC genotype in patients with DHF was compared to those with dengue fever (OR=1.9, p=0.034). Moreover, the presence of the CTLA-4 +49 G allele and TGFbeta1 -509 CC genotype increased the susceptibility to risk of DHF (OR=2.1, p=0.028) and significantly higher virus load (p=0.013). This finding suggests that a combination of CTLA-4 and TGFbeta1 polymorphisms is associated with the susceptibility of DHF and higher virus load
|
650 |
|
4 |
|a Journal Article
|
650 |
|
4 |
|a Research Support, Non-U.S. Gov't
|
650 |
|
7 |
|a Antigens, CD
|2 NLM
|
650 |
|
7 |
|a CTLA-4 Antigen
|2 NLM
|
650 |
|
7 |
|a CTLA4 protein, human
|2 NLM
|
650 |
|
7 |
|a Transforming Growth Factor beta1
|2 NLM
|
700 |
1 |
|
|a Wang, Lin
|e verfasserin
|4 aut
|
700 |
1 |
|
|a Cheng, Jiin-Tsuey
|e verfasserin
|4 aut
|
700 |
1 |
|
|a Chuang, Hau
|e verfasserin
|4 aut
|
700 |
1 |
|
|a Chang, Jen-Chieh
|e verfasserin
|4 aut
|
700 |
1 |
|
|a Liu, Jien-Wei
|e verfasserin
|4 aut
|
700 |
1 |
|
|a Lin, I-Chun
|e verfasserin
|4 aut
|
700 |
1 |
|
|a Yang, Kuender D
|e verfasserin
|4 aut
|
773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 131(2009), 3 vom: 01. Juni, Seite 404-9
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
|
773 |
1 |
8 |
|g volume:131
|g year:2009
|g number:3
|g day:01
|g month:06
|g pages:404-9
|
856 |
4 |
0 |
|u http://dx.doi.org/10.1016/j.clim.2009.01.015
|3 Volltext
|
912 |
|
|
|a GBV_USEFLAG_A
|
912 |
|
|
|a SYSFLAG_A
|
912 |
|
|
|a GBV_NLM
|
912 |
|
|
|a GBV_ILN_11
|
912 |
|
|
|a GBV_ILN_24
|
912 |
|
|
|a GBV_ILN_350
|
951 |
|
|
|a AR
|
952 |
|
|
|d 131
|j 2009
|e 3
|b 01
|c 06
|h 404-9
|