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Article ; Online: Development and Optimization of Bifunctional Fusion Proteins to Locally Modulate Complement Activation in Diseased Tissue.

Fahnoe, Kelly C / Liu, Fei / Morgan, Jennifer G / Ryan, Sarah T / Storek, Michael / Stark, Ellen Garber / Taylor, Fred R / Holers, V Michael / Thurman, Joshua M / Wawersik, Stefan / Kalled, Susan L / Violette, Shelia M

Frontiers in immunology

2022 Volume 13, Page(s) 869725

Abstract: Sustained complement activation is an underlying pathologic driver in many inflammatory and autoimmune diseases. Currently approved anti-complement therapies are directed at the systemic blockade of complement. Consequently, these therapies provide ... ...

Abstract	Sustained complement activation is an underlying pathologic driver in many inflammatory and autoimmune diseases. Currently approved anti-complement therapies are directed at the systemic blockade of complement. Consequently, these therapies provide widespread inhibition of complement pathway activity, beyond the site of ongoing activation and the intended pharmacodynamic (PD) effects. Given the essential role for complement in both innate and adaptive immunity, there is a need for therapies that inhibit complement in diseased tissue while limiting systemic blockade. One potential approach focuses on the development of novel fusion proteins that enable tissue-targeted delivery of complement negative regulatory proteins. These therapies are expected to provide increased potency and prolonged tissue PD, decreased dosing frequency, and the potential for improved safety profiles. We created a library of bifunctional fusion proteins that direct a fragment of the complement negative regulator, complement receptor type 1 (CR1) to sites of tissue injury. Tissue targeting is accomplished through the binding of the fusion protein to complement C3 fragments that contain a surface-exposed C3d domain and which are covalently deposited on tissues where complement is being activated. To that end, we generated a fusion protein that contains an anti-C3d monoclonal antibody recombinantly linked to the first 10 consensus repeats of CR1 (CR1
MeSH term(s)	Antibodies, Monoclonal ; Autoimmune Diseases ; Complement Activation ; Complement C3 ; Humans ; Receptors, Complement/metabolism
Chemical Substances	Antibodies, Monoclonal ; Complement C3 ; Receptors, Complement
Language	English
Publishing date	2022-06-16
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.869725
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Article ; Online: Randomized Phase IIa Clinical Study of an Anti-α

Raghu, Ganesh / Mouded, Majd / Prasse, Antje / Stebbins, Christopher / Zhao, Guolin / Song, Guochen / Arefayene, Million / Violette, Shelia M / Gallagher, Diana / Gibson, Kevin F

American journal of respiratory and critical care medicine

2022 Volume 206, Issue 9, Page(s) 1166–1168

MeSH term(s)	Humans ; Antibodies, Monoclonal ; Antigens, Neoplasm ; Idiopathic Pulmonary Fibrosis ; Transforming Growth Factor beta
Chemical Substances	Antibodies, Monoclonal ; Antigens, Neoplasm ; Transforming Growth Factor beta
Language	English
Publishing date	2022-07-08
Publishing country	United States
Document type	Clinical Trial, Phase II ; Letter ; Randomized Controlled Trial
ZDB-ID	1180953-x
ISSN	1535-4970 ; 0003-0805 ; 1073-449X
ISSN (online)	1535-4970
ISSN	0003-0805 ; 1073-449X
DOI	10.1164/rccm.202205-0868LE
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Article ; Online: C3d-Targeted factor H inhibits tissue complement in disease models and reduces glomerular injury without affecting circulating complement.

Liu, Fei / Ryan, Sarah T / Fahnoe, Kelly C / Morgan, Jennifer G / Cheung, Anne E / Storek, Michael J / Best, Alejandro / Chen, Hui A / Locatelli, Monica / Xu, Shuyun / Schmidt, Enno / Schmidt-Jiménez, Leon F / Bieber, Katja / Henderson, Joel M / Lian, Christine G / Verschoor, Admar / Ludwig, Ralf J / Benigni, Ariela / Remuzzi, Giuseppe /

Salant, David J / Kalled, Susan L / Thurman, Joshua M / Holers, V Michael / Violette, Shelia M / Wawersik, Stefan

Molecular therapy : the journal of the American Society of Gene Therapy

2024 Volume 32, Issue 4, Page(s) 1061–1079

Abstract: Complement-mediated diseases can be treated using systemic inhibitors. However, complement components are abundant in circulation, affecting systemic inhibitors' exposure and efficacy. Furthermore, because of complement's essential role in immunity, ... ...

Abstract	Complement-mediated diseases can be treated using systemic inhibitors. However, complement components are abundant in circulation, affecting systemic inhibitors' exposure and efficacy. Furthermore, because of complement's essential role in immunity, systemic treatments raise infection risk in patients. To address these challenges, we developed antibody fusion proteins combining the alternative-pathway complement inhibitor factor H (fH
MeSH term(s)	Humans ; Mice ; Rats ; Animals ; Complement Factor H/genetics ; Complement C3d/metabolism ; Kidney Diseases/etiology ; Antibodies ; Complement Activation
Chemical Substances	Complement Factor H (80295-65-4) ; Complement C3d (80295-45-0) ; Antibodies
Language	English
Publishing date	2024-02-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2010592-7
ISSN	1525-0024 ; 1525-0016
ISSN (online)	1525-0024
ISSN	1525-0016
DOI	10.1016/j.ymthe.2024.02.001
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Article: The αvβ6 integrin in cancer cell-derived small extracellular vesicles enhances angiogenesis.

Krishn, Shiv Ram / Salem, Israa / Quaglia, Fabio / Naranjo, Nicole M / Agarwal, Ekta / Liu, Qin / Sarker, Srawasti / Kopenhaver, Jessica / McCue, Peter A / Weinreb, Paul H / Violette, Shelia M / Altieri, Dario C / Languino, Lucia R

Journal of extracellular vesicles

2020 Volume 9, Issue 1, Page(s) 1763594

Abstract: Prostate cancer (PrCa) cells crosstalk with the tumour microenvironment by releasing small extracellular vesicles (sEVs). sEVs, as well as large extracellular vesicles (LEVs), isolated via iodixanol density gradients from PrCa cell culture media, express ...

Abstract	Prostate cancer (PrCa) cells crosstalk with the tumour microenvironment by releasing small extracellular vesicles (sEVs). sEVs, as well as large extracellular vesicles (LEVs), isolated via iodixanol density gradients from PrCa cell culture media, express the epithelial-specific αvβ6 integrin, which is known to be induced in cancer. In this study, we show sEV-mediated protein transfer of αvβ6 integrin to microvascular endothelial cells (human microvascular endothelial cells 1 - HMEC1) and demonstrate that
Language	English
Publishing date	2020-05-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2683797-3
ISSN	2001-3078
ISSN	2001-3078
DOI	10.1080/20013078.2020.1763594
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Article ; Online: Blocking TGFβ via Inhibition of the αvβ6 Integrin: A Possible Therapy for Systemic Sclerosis Interstitial Lung Disease.

Katsumoto, Tamiko R / Violette, Shelia M / Sheppard, Dean

International journal of rheumatology

2011 Volume 2011, Page(s) 208219

Abstract: Interstitial lung disease (ILD) is a commonly encountered complication of systemic sclerosis (SSc) and accounts for a significant proportion of SSc-associated morbidity and mortality. Its pathogenesis remains poorly understood, and therapies that treat ... ...

Abstract	Interstitial lung disease (ILD) is a commonly encountered complication of systemic sclerosis (SSc) and accounts for a significant proportion of SSc-associated morbidity and mortality. Its pathogenesis remains poorly understood, and therapies that treat SSc ILD are suboptimal, at best. SSc ILD pathogenesis may share some common mechanisms with other fibrotic lung diseases, in which dysregulation of lung epithelium can contribute to pathologic fibrosis via recruitment or in situ generation and activation of fibroblasts. TGFβ, a master regulator of fibrosis, is tightly regulated in the lung by the integrin αvβ6, which is expressed at low levels on healthy alveolar epithelial cells but is highly induced in the setting of lung injury or fibrosis. Here we discuss the biology of αvβ6 and present this integrin as a potentially attractive target for inhibition in the setting of SSc ILD.
Language	English
Publishing date	2011-10-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	2503284-7
ISSN	1687-9279 ; 1687-9260
ISSN (online)	1687-9279
ISSN	1687-9260
DOI	10.1155/2011/208219
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Article ; Online: A Phase IIb Randomized Clinical Study of an Anti-α

American journal of respiratory and critical care medicine

2022 Volume 206, Issue 9, Page(s) 1128–1139

Abstract: Rationale: ...

Abstract	Rationale:
MeSH term(s)	Humans ; Idiopathic Pulmonary Fibrosis/drug therapy ; Antibodies, Monoclonal/therapeutic use ; Treatment Outcome ; Double-Blind Method ; Immunoglobulin G
Chemical Substances	Antibodies, Monoclonal ; Immunoglobulin G
Language	English
Publishing date	2022-06-30
Publishing country	United States
Document type	Randomized Controlled Trial ; Journal Article
ZDB-ID	1180953-x
ISSN	1535-4970 ; 0003-0805 ; 1073-449X
ISSN (online)	1535-4970
ISSN	0003-0805 ; 1073-449X
DOI	10.1164/rccm.202112-2824OC
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Article ; Online: The coagulation system contributes to alphaVbeta6 integrin expression and liver fibrosis induced by cholestasis.

Sullivan, Bradley P / Weinreb, Paul H / Violette, Shelia M / Luyendyk, James P

The American journal of pathology

2010 Volume 177, Issue 6, Page(s) 2837–2849

Abstract: Chronic injury to intrahepatic bile duct epithelial cells (BDECs) elicits expression of various mediators, including the αVβ6 integrin, promoting liver fibrosis. We tested the hypothesis that tissue factor (TF)-dependent thrombin generation and protease ... ...

Abstract	Chronic injury to intrahepatic bile duct epithelial cells (BDECs) elicits expression of various mediators, including the αVβ6 integrin, promoting liver fibrosis. We tested the hypothesis that tissue factor (TF)-dependent thrombin generation and protease activated receptor-1 (PAR-1) activation contribute to liver fibrosis induced by cholestasis via induction of αVβ6 expression. To test this hypothesis, mice deficient in either TF or PAR-1 were fed a diet containing 0.025% α-naphthylisothiocyanate (ANIT), a BDEC-selective toxicant. In genetically modified mice with a 50% reduction in liver TF activity fed an ANIT diet, coagulation cascade activation and liver fibrosis were reduced. Similarly, liver fibrosis was significantly reduced in PAR-1(-/-) mice fed an ANIT diet. Hepatic integrin β6 mRNA induction, expression of αVβ6 protein by intrahepatic BDECs, and SMAD2 phosphorylation were reduced by TF deficiency and PAR-1 deficiency in mice fed the ANIT diet. Treatment with either an anti-αVβ6 blocking antibody or soluble transforming growth factor-β receptor type II reduced liver fibrosis in mice fed the ANIT diet. PAR-1 activation enhanced transforming growth factor-β1-induced integrin β6 mRNA expression in both transformed human BDECs and primary rat BDECs. Interestingly, TF and PAR-1 mRNA levels were increased in livers from patients with cholestatic liver disease. These results indicate that a TF-PAR-1 pathway contributes to liver fibrosis induced by chronic cholestasis by increasing expression of the αVβ6 integrin, an important regulator of transforming growth factor-β1 activation.
MeSH term(s)	Adult ; Aged ; Animals ; Bile Ducts, Intrahepatic/metabolism ; Bile Ducts, Intrahepatic/pathology ; Blood Coagulation Factors/physiology ; Cells, Cultured ; Cholestasis/complications ; Cholestasis/genetics ; Cholestasis/metabolism ; Female ; Gene Expression ; Humans ; Integrin alphaV/genetics ; Integrin alphaV/metabolism ; Integrin beta Chains/genetics ; Integrin beta Chains/metabolism ; Liver Cirrhosis/etiology ; Liver Cirrhosis/genetics ; Liver Cirrhosis/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Middle Aged ; Rats ; Receptor, PAR-1/genetics ; Receptor, PAR-1/metabolism ; Receptor, PAR-1/physiology ; Thromboplastin/genetics ; Thromboplastin/metabolism ; Thromboplastin/physiology
Chemical Substances	Blood Coagulation Factors ; Integrin alphaV ; Integrin beta Chains ; Receptor, PAR-1 ; integrin beta6 ; Thromboplastin (9035-58-9)
Language	English
Publishing date	2010-10-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.2353/ajpath.2010.100425
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Article ; Online: Inhibition of integrin α

Olof Olsson, P / Gustafsson, Renata / Salnikov, Alexei V / Göthe, Maria / Zeller, Kathrin S / Friman, Tomas / Baldetorp, Bo / Koopman, Louise A / Weinreb, Paul H / Violette, Shelia M / Kalamajski, Sebastian / Heldin, Nils-Erik / Rubin, Kristofer

Cell communication and signaling : CCS

2018 Volume 16, Issue 1, Page(s) 36

Abstract: Background: Chemotherapeutic efficacy can be improved by targeting the structure and function of the extracellular matrix (ECM) in the carcinomal stroma. This can be accomplished by e.g. inhibiting TGF-β1 and -β3 or treating with Imatinib, which results ...

Abstract	Background: Chemotherapeutic efficacy can be improved by targeting the structure and function of the extracellular matrix (ECM) in the carcinomal stroma. This can be accomplished by e.g. inhibiting TGF-β1 and -β3 or treating with Imatinib, which results in scarcer collagen fibril structure in xenografted human KAT-4/HT29 (KAT-4) colon adenocarcinoma. Methods: The potential role of α Results: Both KAT-4 and Capan-2 cells expressed the α Conclusion: Our data demonstrate that the α
MeSH term(s)	Animals ; Antibodies, Monoclonal/immunology ; Antigens, Neoplasm/immunology ; Antigens, Neoplasm/metabolism ; Cell Line, Tumor ; Cell Transformation, Neoplastic ; Collagen/chemistry ; Collagen/metabolism ; Extracellular Fluid/metabolism ; Female ; Gene Expression Profiling ; Humans ; Integrins/immunology ; Integrins/metabolism ; Mice ; Pressure ; Transforming Growth Factor beta/metabolism
Chemical Substances	Antibodies, Monoclonal ; Antigens, Neoplasm ; Integrins ; Transforming Growth Factor beta ; integrin alphavbeta6 ; Collagen (9007-34-5)
Language	English
Publishing date	2018-07-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1478-811X
ISSN (online)	1478-811X
DOI	10.1186/s12964-018-0249-7
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Article ; Online: αvβ6 integrin is required for TGFβ1-mediated matrix metalloproteinase2 expression.

Dutta, Anindita / Li, Jing / Fedele, Carmine / Sayeed, Aejaz / Singh, Amrita / Violette, Shelia M / Manes, Thomas D / Languino, Lucia R

The Biochemical journal

2015 Volume 466, Issue 3, Page(s) 525–536

Abstract: Transforming growth factor (TGF) β1 activity depends on a complex signalling cascade that controls expression of several genes. Among others, TGFβ1 regulates expression of matrix metalloproteinases (MMPs) through activation of Smads. In the present study, ...

Abstract	Transforming growth factor (TGF) β1 activity depends on a complex signalling cascade that controls expression of several genes. Among others, TGFβ1 regulates expression of matrix metalloproteinases (MMPs) through activation of Smads. In the present study, we demonstrate for the first time that the αvβ6 integrin interacts with TGFβ receptor II (TβRII) through the β6 cytoplasmic domain and promotes Smad3 activation in prostate cancer (PrCa) cells. Another related αv integrin, αvβ5, as well as the αvβ6/3 integrin, which contains a chimeric form of β6 with a β3 cytoplasmic domain, do not associate with TβRII and fail to show similar responses. We provide evidence that αvβ6 is required for up-regulation of MMP2 by TGFβ1 through a Smad3-mediated transcriptional programme in PrCa cells. The functional relevance of these results is underscored by the finding that αvβ6 modulates cell migration in an MMP2-dependent manner on an αvβ6-specific ligand, latency-associated peptide (LAP)-TGFβ. Overall, these mechanistic studies establish that expression of a single integrin, αvβ6, is sufficient to promote activation of Smad3, regulation of MMP2 levels and consequent catalytic activity, as well as cell migration. Our study describes a new TGFβ1-αvβ6-MMP2 signalling pathway that, given TGFβ1 pro-metastatic activity, may have profound implications for PrCa therapy.
MeSH term(s)	Antigens, Neoplasm/metabolism ; Cell Line, Tumor ; Cell Movement/drug effects ; Cell Movement/physiology ; Gene Expression Regulation, Enzymologic ; Humans ; Integrins/metabolism ; Male ; Matrix Metalloproteinase 2/biosynthesis ; Transforming Growth Factor beta1/pharmacology
Chemical Substances	Antigens, Neoplasm ; Integrins ; TGFB1 protein, human ; Transforming Growth Factor beta1 ; integrin alphavbeta6 ; MMP2 protein, human (EC 3.4.24.24) ; Matrix Metalloproteinase 2 (EC 3.4.24.24)
Language	English
Publishing date	2015-03-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2969-5
ISSN	1470-8728 ; 0006-2936 ; 0306-3275 ; 0264-6021
ISSN (online)	1470-8728
ISSN	0006-2936 ; 0306-3275 ; 0264-6021
DOI	10.1042/BJ20140698
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Article ; Online: αvβ6 integrin may be a potential prognostic biomarker in interstitial lung disease.

Saini, Gauri / Porte, Joanne / Weinreb, Paul H / Violette, Shelia M / Wallace, William A / McKeever, Tricia M / Jenkins, Gisli

The European respiratory journal

2015 Volume 46, Issue 2, Page(s) 486–494

Abstract: Idiopathic pulmonary fibrosis (IPF) and fibrotic nonspecific interstitial pneumonitis are progressive interstitial lung diseases (ILDs) with limited treatment options and poor survival. However, the rate of disease progression is variable, implying there ...

Abstract	Idiopathic pulmonary fibrosis (IPF) and fibrotic nonspecific interstitial pneumonitis are progressive interstitial lung diseases (ILDs) with limited treatment options and poor survival. However, the rate of disease progression is variable, implying there may be different endotypes of disease. We hypothesised that immunophenotyping biopsies from ILD patients might reveal distinct endotypes of progressive fibrotic disease, which may facilitate stratification when undertaking clinical trials of novel therapies for IPF.43 paraffin-embedded, formalin-fixed lung tissue sections were immunostained for five molecules implicated in the pathogenesis of the fibrosis: α-smooth muscle actin (αSMA), αvβ6 integrin, pro-surfactant protein C (SP-C), hepatocyte growth factor (HGF) and tenascin-C (TenC). Levels of immunostaining and numbers of fibroblastic foci were quantified using operator-dependent and -independent methods. The relationship of all these markers to overall survival was analysed.Staining revealed high levels of αSMA, αvβ6 integrin, pro-SP-C, HGF and TenC, and fibroblastic foci. Immunostaining varied across samples for all molecules but only the extent of αvβ6 integrin immunostaining was associated with increased mortality. There was no association with the other markers measured.Our data suggest high levels of αvβ6 integrin may identify a specific endotype of progressive fibrotic lung disease.
MeSH term(s)	Adult ; Aged ; Antigens, Neoplasm/metabolism ; Biomarkers/metabolism ; Biopsy ; Female ; Humans ; Integrins/metabolism ; Lung/pathology ; Lung Diseases, Interstitial/pathology ; Lung Diseases, Interstitial/surgery ; Male ; Middle Aged ; Prognosis
Chemical Substances	Antigens, Neoplasm ; Biomarkers ; Integrins ; integrin alphavbeta6
Language	English
Publishing date	2015-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639359-7
ISSN	1399-3003 ; 0903-1936
ISSN (online)	1399-3003
ISSN	0903-1936
DOI	10.1183/09031936.00210414
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