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-CD20–mediated 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 CX 3 CR1 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 CX 3 CR1 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: CX 3 CR1-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
Journal of Clinical Investigation