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231224s2011 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2011.04.018
|2 doi
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|a pubmed25n0696.xml
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|a DE-627
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|e rakwb
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|a eng
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|a Das, Arpita
|e verfasserin
|4 aut
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|a Simian immunodeficiency virus infection in rhesus macaques induces selective tissue specific B cell defects in double positive CD21+CD27+ memory B cells
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|c 2011
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
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|2 rdacarrier
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|a Date Completed 19.10.2011
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|a Date Revised 16.04.2024
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2011 Elsevier Inc. All rights reserved.
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|a B cell dysfunction represents a central feature in HIV infection and pathogenesis. Our recent studies have shown that peripheral and lymphoid double positive CD21+CD27+ B cells were able to become activated and proliferate at higher rates than other B cell subpopulations. Increased proliferation of tonsillar memory B cells was identified compared to other tissues examined. Here, we demonstrate the decreased proliferation of tonsillar memory (CD21+CD27+) B cells during acute SIV infection also suggests that these cells may play an important role in SIV pathogenesis. Our findings demonstrate that SIV infection may induce selective defective responses in specific tissues, by suppressing memory B cell proliferation in tissues
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|a Journal Article
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|a Research Support, N.I.H., Extramural
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|a Research Support, Non-U.S. Gov't
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|a Receptors, Complement 3d
|2 NLM
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|a Tumor Necrosis Factor Receptor Superfamily, Member 7
|2 NLM
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|a Veazey, Ronald S
|e verfasserin
|4 aut
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|a Wang, Xiaolei
|e verfasserin
|4 aut
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|a Lackner, Andrew A
|e verfasserin
|4 aut
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|a Xu, Huanbin
|e verfasserin
|4 aut
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|a Pahar, Bapi
|e verfasserin
|4 aut
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 140(2011), 3 vom: 02. Sept., Seite 223-8
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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|g volume:140
|g year:2011
|g number:3
|g day:02
|g month:09
|g pages:223-8
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|u http://dx.doi.org/10.1016/j.clim.2011.04.018
|3 Volltext
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