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Effects of IFN-γ on immune cell kinetics during the resolution of acute lung injury.

The immunologic responses that occur early in the acute respiratory distress syndrome (ARDS) elicit immune-mediated damage. The mechanisms underlying the resolution of ARDS, particularly the role of signaling molecules in regulating immune cell kinetics, remain important questions. Th1-mediated responses can contribute to the pathogenesis of acute lung injury (ALI). Interferon-gamma (IFN-γ) orchestrates early inflammatory events, enhancing immune-mediated damage. The current study investigated IFN-γ during resolution in several experimental models of ALI. The absence of IFN-γ resulted in altered kinetics of lymphocyte and macrophage responses, suggesting that IFN-γ present in this microenvironment is influential in ALI resolution. Genetic deficiency of IFN-γ or administering neutralizing IFN-γ antibodies accelerated the pace of resolution. Neutralizing IFN-γ decreased the numbers of interstitial and inflammatory macrophages and increased alveolar macrophage numbers during resolution. Our results underline the complexity of lung injury resolution and provide insight into the effects through which altered IFN-γ concentrations affect immune cell kinetics and the rate of resolution. These findings suggest that therapies that spatially or temporally control IFN-γ signaling may promote ALI resolution. Identifying and elucidating the mechanisms critical to ALI resolution will allow the development of therapeutic approaches to minimize collateral tissue damage without adversely altering the response to injury.

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Erratum to: Repertoire and Neutralizing Activity of Antibodies Against Hepatitis C Virus E2 Peptide in Patients With Spontaneous Resolution of Hepatitis C.


2595 related Products with: Erratum to: Repertoire and Neutralizing Activity of Antibodies Against Hepatitis C Virus E2 Peptide in Patients With Spontaneous Resolution of Hepatitis C.

Hepatitis C Virus antibod Rabbit Anti-Hepatitis C V Rabbit Anti-Hepatitis C V Rabbit Anti-Polyprotein(H Rabbit Anti-Polyprotein(H HbcAg - Hepatitis B Viru Hepatitis A Virus antibod Rabbit Anti-Hepatitis C V Mouse Anti-Hepatitis A Vi Rabbit Anti-Hepatitis C V Rabbit Anti-Hepatitis C V Rabbit Anti-Polyprotein(H

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Novel antibodies targeting the N-terminus of FGF19 inhibit hepatocellular carcinoma growth without bile-acid-related side effects.

Hepatocellular carcinoma (HCC) is a common and particularly fatal form of cancer for which very few drugs are effective. The fibroblast growth factor 19 (FGF19) has been viewed as a driver of HCC development and a potential antibody target for developing novel HCC therapy. However, a previously developed anti-FGF19 antibody disrupted FGF19's normal regulatory function and caused severe bile-acid-related side effects despite of having potent anti-tumor effects in preclinical models. Here, we developed novel human antibodies (G1A8 and HS29) that specifically target the N-terminus of FGF19. Both antibodies inhibited FGF19-induced HCC cell proliferation in vitro and significantly suppressed HCC tumor growth in mouse models. Importantly, no bile-acid-related side effects were observed in preclinical cynomolgus monkeys. Fundamentally, our study demonstrates that it is possible to target FGF19 for anti-HCC therapies without adversely affecting its normal bile-acid-regulatory function, and highlights the exciting promise of G1A8 or HS29 as potential therapy for HCC.

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