Immune Regulation News Volume 4.20 | Jun 1 2012

Inhibitory Receptors Bind ANGPTLs and Support Blood Stem Cells and Leukaemia Development
Researchers found that the immune-inhibitory receptor human leukocyte immunoglobulin-like receptor B2 and its mouse orthologue paired immunoglobulin-like receptor are receptors for several Angiopoietin-like proteins (ANGPTLs). [Nature] Abstract | Press Release

Regulation of Type 2 Helper T Cell Development by CXCR5⁺ Dendritic Cells and Lymphotoxin-Expressing B Cells
Researchers found that, after infection with an intestinal nematode, antigen-bearing dendritic cells and CD4⁺ T cells upregulated the chemokine receptor CXCR5 and localized together outside the T cell zone by a mechanism dependent on the chemokine CXCL13, B cells and lymphotoxin. [Nat Immunol]
Abstract | Press Release

TGF-β Signaling to T Cells Inhibits Autoimmunity during Lymphopenia-Driven Proliferation
When researchers deleted the receptor for transforming growth factor-β (TGF-β) through the use of Cre driven by a promoter that is active much later in T cell development, adult mice in which most peripheral CD4⁺ or CD8⁺ T cells lacked the receptor for TGF-β showed no signs of autoimmunity. [Nat Immunol] Abstract

Live Imaging of Tumor Initiation in Zebrafish Larvae Reveals a Trophic Role for Leukocyte-Derived Prostaglandin E₂
Researchers took advantage of the translucency and genetic tractability of zebrafish larvae to investigate the involvement of inflammatory cells at cancer initiation, when transformed cells first arise in tissues. [Curr Biol] Abstract

C/EBP Homologous Protein Contributes to Cytokine-Induced Pro-Inflammatory Responses and Apoptosis in β-Cells
Data suggest that the C/EBP homologous protein (CHOP) has a dual role in promoting β-cell death: CHOP directly contributes to cytokine-induced β-cell apoptosis by promoting cytokine-induced mitochondrial pathways of apoptosis; and, by supporting the NF-κB activation and subsequent cytokine/chemokine expression, CHOP may contribute to apoptosis and the chemo attraction of mononuclear cells to the islets during insulitis. [Cell Death Differ] Abstract

Loss of Mucosal CD103+ Dendritic Cells and IL-17+ and IL-22+ Lymphocytes Is Associated with Mucosal Damage in SIV Infection
By investigating alterations in mucosal immunity during Simian immunodeficiency virus (SIV) infection, researchers found that damage to the colonic epithelial barrier was associated with loss of multiple lineages of interleukin (IL)-17-producing lymphocytes, cells that microarray analysis showed expressed genes important for enterocyte homeostasis, including IL-22. [Mucosal Immunol] Abstract

NKT Cells Stimulated by Long Fatty Acyl Chain Sulfatides Significantly Reduces the Incidence of Type 1 Diabetes in Nonobese Diabetic Mice
Data suggest that C24:0 stimulated type II NKT cells may regulate protection from T1D by activating DCs to secrete IL-10 and suppress the activation and expansion of type I iNKT cells and diabetogenic T cells. [PLoS One] Full Article

Mincle Polarizes Human Monocyte and Neutrophil Responses to Candida albicans
This study identified an unusual pattern of reciprocal expression of Mincle on peripheral blood monocytes or neutrophils isolated from the same donor. [Immunol Cell Biol] Abstract

 

IMMUNE Pharmaceuticals Announces Strategic Partnership with the World-Renowned Weizmann Institute
IMMUNE Pharmaceuticals and Yeda, the technology transfer company of the Weizmann Institute of Science, announced a broad collaboration to develop antibody therapeutics targeting HER3, one of the most promising novel targets in oncology with early clinical validation. [IMMUNE Pharmaceuticals] Press Release

Bristol-Myers Squibb Announces Global Collaboration with Leading Academic Institutions to Advance Science of Immuno-Oncology
Bristol-Myers Squibb Company announced the formation of the International Immuno-Oncology Network, a global collaboration between industry and academia that aims to further the scientific understanding of immuno-oncology. [Bristol-Myers Squibb Company] Press Release

UCI Stem Cell Researcher to Receive $4.8 Million in State Funding
A University of California, Irvine (UCI) immunologist will receive $4.8 million to create a new line of neural stem cells that can be used to treat multiple sclerosis. [University of California, Irvine] Press Release

City of Hope Receives $5 Million Grant to Develop T Cell Treatment Targeting Brain Tumor Stem Cells
City of Hope was granted a $5,217,004 early translational research award by the California Institute for Regenerative Medicine to support the development of a T cell-based immunotherapy that re-directs a patient’s own immune response against glioma stem cells. [City of Hope] Press Release

White House Petitioned to Make Research Free to Access
More than 17,000 people have signed an online petition urging US President Barack Obama to require all scientific journal articles resulting from US taxpayer-funded research to be made freely available online. [White House, United States] Press Release

Horizon 2020: A €80 Billion Battlefield for Open Access
As negotiations proceed to shape the next installment of Europe’s gargantuan research funding programs, scientists, librarians, and publishers are eagerly awaiting the answer to a critical question: How strong will the new seven-year program, called Horizon 2020, be on Open Access? [European Commission, European Union] Press Release

National Institutes of Health (United States)

Food and Drug Administration (United States)

Center for Biologics Evaluation and Research (United States)

European Medicines Agency (European Union)

Medicines and Healthcare Products Regulatory Agency (United Kingdom)

Therapeutic Goods Administration (Australia)

NEW Federation of Clinical Immunology Societies (FOCiS) 2012
June 20-23, 2012
Vancouver, Canada

Visit our events page to see a complete list of events in the immune regulation community.

Have we missed an important article or publication in Immune Regulation News? Click here to submit!

Comments or Suggestions? Email info@connexoncreative.com with your feedback.