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PUBLIC RELEASE DATE: 1-Nov-2013
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press_releases@the-jci.org
Journal of Clinical Investigation
Liver tropism is key for B cell deletion immunotherapy
Antibodies against the B cell surface protein CD20 have been used successfully to treat B cell-mediated autoimmune diseases and lymphomas. Antibody binding receptors, called Fc receptors, on other immune cells bind anti-CD20 on coated B cells, which induces B cell deletion through a mechanism that is not clearly understood. In this issue of the Journal of Clinical Investigation, Philippe Bousse and colleagues at the Pasteur Institute in Paris described the fate of B cells in live mice after treatment with anti-CD20 antibodies. Bousse and his group found that B cells circulating through the liver were the first ones depleted after treatment and that B cells in circulation were more susceptible to deletion than those stationary in the spleen or lymph nodes. The researchers used intravital two-photon microscopy to follow B cells in the liver as they halted near specialized Fc receptor-bearing cells called Kupffer cells. The Kupffer cells bound and consumed the anti-CD20-coated B cells. The study assigns a vital role to liver Kupffer cells in deleting B cells and describes techniques that may be used to improve the effectiveness of anti-CD20 therapy
TITLE:
The mechanism of anti-CD20mediated B cell depletion revealed by intravital imaging
AUTHOR CONTACT:
Philippe Bousso
Institut Pasteur, Paris, , FRA
Phone: 33 1 45 68 85 51; Fax: ; E-mail: bousso@pasteur.fr
View this article at: http://www.jci.org/articles/view/70972?key=b0390c54a360d17753f4
Dysfunctional chemokine receptor promotes candidiasis
Candida albicans is one of the leading causes of hospital-acquired infections in immune compromised patients. The risk of both developing candidiasis and the clinical outcome of infection is variable among patients, and the host-dependent factors that contribute to patient susceptibility to C. albicans infection are poorly understood. In this issue of the Journal of Clinical Investigation, Michail Lionakis and colleagues at the National Institute of Allergy and Infectious Diseases demonstrated that the chemokine receptor CX3CR1 is required for the interaction of C. albicans and macrophages in the kidney. Mice lacking this receptor were prone to C. albicans-induced kidney failure; however, these mice did not have increased fungal burden in other organs. Furthermore, the authors found that patients with a mutation in the gene encoding CX3CR1 were at higher risk of candidiasis. This study identifies an important role for the interaction of C. albicans and macrophages in disease progression and outcome.
TITLE:
CX3CR1-dependent renal macrophage survival promotes Candida control and host survival
AUTHOR CONTACT:
Michail Lionakis
NIAID NIH, Bethesda, MD, USA
Phone: 301-443-5089; Fax: 301-480-5787; E-mail: lionakism@mail.nih.gov
View this article at: http://www.jci.org/articles/view/71307?key=c09c9f7b1f8d1860c357
ALSO IN THIS ISSUE
TITLE:
Retinoblastoma protein prevents enteric nervous system defects and intestinal pseudo-obstruction
AUTHOR CONTACT:
Robert Heuckeroth
The Children's Hospital of Philadelphia Research Institute, Philadelphia, PA, USA
Phone: 215-590-1209; E-mail: heuckerothr@email.chop.edu
View this article at: http://www.jci.org/articles/view/67653?key=ec84fac40d09ca365af6
TITLE:
Transmembrane protein ESDN promotes endothelial VEGF signaling and regulates angiogenesis
AUTHOR CONTACT:
Mehran Sadeghi
Yale University, West Haven, CT, USA
Phone: 203-932 5711 x3398; E-mail: mehran.sadeghi@yale.edu
View this article at: http://www.jci.org/articles/view/67752?key=b36f90578e3cb5cdd212
TITLE:
Apelin is a positive regulator of ACE2 in failing hearts
AUTHOR CONTACT:
Keiji Kuba
Akita University Graduate School of Medicine, Akita, , JPN
Phone: +81-18-884-6067; Fax: ; E-mail: kuba@med.akita-u.ac.jp
View this article at: http://www.jci.org/articles/view/69608?key=bf375e497b8130dba13e
TITLE:
Serotonin 2C receptors in pro-opiomelanocortin neurons regulate energy and glucose homeostasis
AUTHOR CONTACT:
Joel K. Elmquist
UT Southwestern Medical Center, Dallas, TX, USA
Phone: 214 648 2911; Fax: 214 648 5612; E-mail: joel.elmquist@utsouthwestern.edu
View this article at: http://www.jci.org/articles/view/70338?key=6df71b0a99bbfa2f1df6
TITLE:
Enhanced autophagy ameliorates cardiac proteinopathy
AUTHOR CONTACT:
Jeffrey Robbins
Cincinnati Childrens Hosp, Cincinnati, OH, USA
Phone: 5136368098; Fax: 5136385859; E-mail: jeff.robbins@cchmc.org
View this article at: http://www.jci.org/articles/view/70877?key=78dacdec9743e32334d8
TITLE:
Insulin receptor substrate signaling suppresses neonatal autophagy in the heart
AUTHOR CONTACT:
E. Dale Abel
University of Utah School of Medicine, Salt Lake City, UT, USA
Phone: 801 585-0727; Fax: 801 585-0701; E-mail: dale.abel@hmbg.utah.edu
View this article at: http://www.jci.org/articles/view/71171?key=9889f254517eee347fc6
###
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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
PUBLIC RELEASE DATE: 1-Nov-2013
[
]
ShareContact: Corinne Williams
press_releases@the-jci.org
Journal of Clinical Investigation
Liver tropism is key for B cell deletion immunotherapy
Antibodies against the B cell surface protein CD20 have been used successfully to treat B cell-mediated autoimmune diseases and lymphomas. Antibody binding receptors, called Fc receptors, on other immune cells bind anti-CD20 on coated B cells, which induces B cell deletion through a mechanism that is not clearly understood. In this issue of the Journal of Clinical Investigation, Philippe Bousse and colleagues at the Pasteur Institute in Paris described the fate of B cells in live mice after treatment with anti-CD20 antibodies. Bousse and his group found that B cells circulating through the liver were the first ones depleted after treatment and that B cells in circulation were more susceptible to deletion than those stationary in the spleen or lymph nodes. The researchers used intravital two-photon microscopy to follow B cells in the liver as they halted near specialized Fc receptor-bearing cells called Kupffer cells. The Kupffer cells bound and consumed the anti-CD20-coated B cells. The study assigns a vital role to liver Kupffer cells in deleting B cells and describes techniques that may be used to improve the effectiveness of anti-CD20 therapy
TITLE:
The mechanism of anti-CD20mediated B cell depletion revealed by intravital imaging
AUTHOR CONTACT:
Philippe Bousso
Institut Pasteur, Paris, , FRA
Phone: 33 1 45 68 85 51; Fax: ; E-mail: bousso@pasteur.fr
View this article at: http://www.jci.org/articles/view/70972?key=b0390c54a360d17753f4
Dysfunctional chemokine receptor promotes candidiasis
Candida albicans is one of the leading causes of hospital-acquired infections in immune compromised patients. The risk of both developing candidiasis and the clinical outcome of infection is variable among patients, and the host-dependent factors that contribute to patient susceptibility to C. albicans infection are poorly understood. In this issue of the Journal of Clinical Investigation, Michail Lionakis and colleagues at the National Institute of Allergy and Infectious Diseases demonstrated that the chemokine receptor CX3CR1 is required for the interaction of C. albicans and macrophages in the kidney. Mice lacking this receptor were prone to C. albicans-induced kidney failure; however, these mice did not have increased fungal burden in other organs. Furthermore, the authors found that patients with a mutation in the gene encoding CX3CR1 were at higher risk of candidiasis. This study identifies an important role for the interaction of C. albicans and macrophages in disease progression and outcome.
TITLE:
CX3CR1-dependent renal macrophage survival promotes Candida control and host survival
AUTHOR CONTACT:
Michail Lionakis
NIAID NIH, Bethesda, MD, USA
Phone: 301-443-5089; Fax: 301-480-5787; E-mail: lionakism@mail.nih.gov
View this article at: http://www.jci.org/articles/view/71307?key=c09c9f7b1f8d1860c357
ALSO IN THIS ISSUE
TITLE:
Retinoblastoma protein prevents enteric nervous system defects and intestinal pseudo-obstruction
AUTHOR CONTACT:
Robert Heuckeroth
The Children's Hospital of Philadelphia Research Institute, Philadelphia, PA, USA
Phone: 215-590-1209; E-mail: heuckerothr@email.chop.edu
View this article at: http://www.jci.org/articles/view/67653?key=ec84fac40d09ca365af6
TITLE:
Transmembrane protein ESDN promotes endothelial VEGF signaling and regulates angiogenesis
AUTHOR CONTACT:
Mehran Sadeghi
Yale University, West Haven, CT, USA
Phone: 203-932 5711 x3398; E-mail: mehran.sadeghi@yale.edu
View this article at: http://www.jci.org/articles/view/67752?key=b36f90578e3cb5cdd212
TITLE:
Apelin is a positive regulator of ACE2 in failing hearts
AUTHOR CONTACT:
Keiji Kuba
Akita University Graduate School of Medicine, Akita, , JPN
Phone: +81-18-884-6067; Fax: ; E-mail: kuba@med.akita-u.ac.jp
View this article at: http://www.jci.org/articles/view/69608?key=bf375e497b8130dba13e
TITLE:
Serotonin 2C receptors in pro-opiomelanocortin neurons regulate energy and glucose homeostasis
AUTHOR CONTACT:
Joel K. Elmquist
UT Southwestern Medical Center, Dallas, TX, USA
Phone: 214 648 2911; Fax: 214 648 5612; E-mail: joel.elmquist@utsouthwestern.edu
View this article at: http://www.jci.org/articles/view/70338?key=6df71b0a99bbfa2f1df6
TITLE:
Enhanced autophagy ameliorates cardiac proteinopathy
AUTHOR CONTACT:
Jeffrey Robbins
Cincinnati Childrens Hosp, Cincinnati, OH, USA
Phone: 5136368098; Fax: 5136385859; E-mail: jeff.robbins@cchmc.org
View this article at: http://www.jci.org/articles/view/70877?key=78dacdec9743e32334d8
TITLE:
Insulin receptor substrate signaling suppresses neonatal autophagy in the heart
AUTHOR CONTACT:
E. Dale Abel
University of Utah School of Medicine, Salt Lake City, UT, USA
Phone: 801 585-0727; Fax: 801 585-0701; E-mail: dale.abel@hmbg.utah.edu
View this article at: http://www.jci.org/articles/view/71171?key=9889f254517eee347fc6
###
[
Share]
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Source: http://www.eurekalert.org/pub_releases/2013-11/joci-jet102513.php
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