Replies to post #329016 on Avid Bioservices Inc (CDMO)

[geocappy1]

Since Oncologie has control of patents my guess would be them

[biopharm]

Looks like some have not known the true value of the IP assets behind the MOA of PS Targeting and Oncologie ready to carry prearranged royalties and milestones breadcrumb like to Avid Bioservices / Peregrine Pharmaceuticals

Linking cellular stress responses to systemic homeostasis
Review Article | Published: 10 October 2018

Linking cellular stress responses to systemic homeostasis
Lorenzo Galluzzi, Takahiro Yamazaki & Guido Kroemer
Nature Reviews Molecular Cell Biology (2018) | Download Citation

Abstract
Mammalian cells respond to stress by activating mechanisms that support cellular functions and hence maintain microenvironmental and organismal homeostasis. Intracellular responses to stress, their regulation and their pathophysiological implications have been extensively studied. However, little is known about the signals that emanate from stressed cells to enable a coordinated adaptive response across tissues, organs and the whole organism. Considerable evidence has now accumulated indicating that the intracellular mechanisms that are activated in response to different stresses — which include the DNA damage response, the unfolded protein response, mitochondrial stress signalling and autophagy — as well as the mechanisms ensuring the proliferative inactivation or elimination of terminally damaged cells — such as cell senescence and regulated cell death — are all coupled with the generation of signals that elicit microenvironmental and/or systemic responses. These signals, which involve changes in the surface of stressed cells and/or the secretion of soluble factors or microvesicles, generally support systemic homeostasis but can also contribute to maladaptation and disease.
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https://www.nature.com/articles/s41580-018-0068-0

The Immunobiology of Receptor Activator for Nuclear Factor Kappa B Ligand and Myeloid-Derived Suppressor Cell Activation in Immunoglobulin G4–Related Sclerosing Cholangitis
Hepatology
Pub Date : 2018-10-09
DOI : 10.1002/hep.30095

Min Lian; Qixia Wang; Xiang Jiang; Jun Zhang; Yiran Wei; Yanmei Li; Bo Li; Weihua Chen; Haiyan Zhang; Qi Miao; Yanshen Peng; Xiao Xiao; Li Sheng; Weici Zhang; Jingyuan Fang; Ruqi Tang; M. Eric Gershwin; Xiong Ma

The primary function of myeloid-derived suppressor cells (MDSCs) is reflected in their immune modulatory role in several immune-mediated diseases. In immunoglobulin G4 (IgG4)–related disease (IgG4-RD), it has been hypothesized that there are selective regulatory defects that lead to a T helper 2 (Th2) bias immune response. Herein we have taken advantage of a large cohort of patients with IgG4-related sclerosing cholangitis (IgG4-SC), the most common extrapancreatic involvement of IgG4-RD, as well as controls consisting of primary sclerosing cholangitis, autoimmune hepatitis, and healthy volunteers, to study MDSCs. We report dramatically increased levels of receptor activator for nuclear factor kappa B ligand (RANKL) expression in serum and liver from patients with IgG4-SC compared to both liver-disease and healthy controls. Moreover, in IgG4-SC liver, RANKL-secreting cells specifically colocalized with cluster of differentiation 38–positive plasma cells and MDSCs, particularly monocytic MDSCs, and express the RANKL receptor in liver. Similarly, the frequency and number of peripheral blood MDSCs were significantly increased. Importantly, serum expression levels of RANKL were inversely correlated with the serum level of gamma-glutamyltransferase but significantly positively correlated with the frequency of MDSCs. Moreover, we confirmed that RANKL induced the expansion and activation of MDSCs through the RANKL/RANK/nuclear factor kappa B signal pathway. Of note, RANKL-treated MDSCs suppressed T-cell proliferation and induced Th2 differentiation. Conclusion: Our data suggest that plasma cell–derived RANKL induces the expansion and activation of MDSCs, which suppress T-cell proliferation and contribute to the Th2-type response characteristic of IgG4-SC. (Hepatology 2018; 00:000-000).

http://m.x-mol.com/paper/770388