Immune Regulation News Volume 6.01 | Jan 17 2014

Targeting the Tumor Microenvironment with Interferon-β Bridges Innate and Adaptive Immune Responses
Investigators armed an antibody (Ab) with interferon-β and observed that it is more potent than the first generation of Ab for controlling Ab-resistant tumors. This strategy controls Ab resistance by rebridging suppressed innate and adaptive immunity in the tumor microenvironment. [Cancer Cell] Full Article

Embryonic and Adult-Derived Resident Cardiac Macrophages Are Maintained through Distinct Mechanisms at Steady State and during Inflammation
The authors identified four populations of cardiac macrophages. At steady state, resident macrophages were primarily maintained through local proliferation. However, after macrophage depletion or during cardiac inflammation, Ly6c^hi monocytes contributed to all four macrophage populations, whereas resident macrophages also expanded numerically through proliferation. [Immunity] Abstract | Press Release

Signaling through the Adaptor Molecule MyD88 in CD4⁺ T Cells Is Required to Overcome Suppression by Regulatory T Cells
Scientists showed that the T cell-specific ablation of MyD88 in mice impairs not only T helper 17 (Th17) cell responses, but also Th1 cell responses. MyD88 relayed signals of Toll-like receptor-induced IL-1, which became dispensable for Th1 cell responses in the absence of T regulatory cells. [Immunity] Abstract

Therapeutic Inflammatory Monocyte Modulation Using Immune-Modifying Microparticles
Investigators showed that infused negatively charged, immune-modifying microparticles, derived from polystyrene, microdiamonds, or biodegradable poly(lactic-co-glycolic) acid, were taken up by inflammatory monocytes, in an opsonin-independent fashion, via the macrophage receptor with collagenous structure. [Sci Transl Med] Abstract | Press Release

Integrin CD11b Positively Regulates TLR4-Induced Signaling Pathways in Dendritic Cells but Not in Macrophages
Researchers report that the integrin α_M (CD11b) positively regulates lipopolysaccharide-induced signaling pathways selectively in myeloid dendritic cells but not in macrophages. In dendritic cells, which express lower levels of CD14 and Toll-like receptor 4 (TLR4) than macrophages, CD11b promotes MyD88-dependent and MyD88-independent signaling pathways. [Nat Commun] Full Article

Mouse and Human Notch-1 Regulate Mucosal Immune Responses
The authors showed that epithelial Notch-1 controls the immune function of the epithelium through crosstalk with the nuclear factor-κB/mitogen-activated protein kinase pathways that, in turn, elicits T-cell responses. [Mucosal Immunol] Abstract

Idd13 Is Involved in Determining Immunoregulatory DN T-Cell Number in NOD Mice
Scientists investigated the impact of major insulin-dependent diabetes (Idd) loci in defining the number of CD4^–CD8^– (double negative, DN) T cells. They demonstrated that although Idd3, Idd5 and Idd9 loci do not regulate DN T-cell number, NOD mice congenic for diabetes resistance alleles at the Idd13 locus show a partial restoration in DN T-cell number. [Genes Immun] Abstract

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Biothera Research Shows Potential for Treating Imprime PGG Biomarker-Negative Cancer Patients
Biothera has enhanced innate immune responses to its cancer immunotherapy drug candidate Imprime PGG® in subjects regardless of biomarker status, demonstrating the opportunity to treat a larger patient population. [Press release from Biothera, the immune health company discussing research presented at the Cambridge Healthtech Institute’s Antibody-Drug Conjugates/Engineering Targeted Therapeutics conference, Palm Springs] Press Release

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Agenus Announces Phase II Checkpoint Inhibitor Combination Trial with Prophage Cancer Vaccine for Melanoma
Agenus Inc. announced initiation of a randomized Phase II trial with Prophage for melanoma, and Bristol-Myers Squibb’s Yervoy^® (ipilimumab) for the treatment of Stage III and IV metastatic melanoma. The combination has the potential to trigger a more effective immune response against the tumor than Yervoy alone. [Agenus Inc.] Press Release

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