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2. FutureMS Cohort Profile: A Scottish Multi-Centre Inception Cohort Study of Relapsing-Remitting Multiple Sclerosis

Author

Hafezi K, Lee Murphy, Peter Foley, Rozanna Meijboom, Chang J, Amy Stenson, Baranzini S, Patrick K. A. Kearns, David M. Hunt, Carod-Artal F, McLeod M, O’Riordan J, Freyer E, Chen Y, Harroud A, Martin S, MacDougall N, Siddharthan Chandran, Elizabeth N. York, Christine Weaver, Adam D. Waldman, and Peter Connick

Subjects
Pediatrics, medicine.medical_specialty, business.industry, Multiple sclerosis, Disease, medicine.disease, INCEPTION COHORT, Relapsing remitting, Cohort, medicine, Biomarker (medicine), Multi centre, business, Cohort study
Abstract

Multiple sclerosis (MS) is an immune-mediated, neuroinflammatory disease of the central nervous system and in industrialised countries is the most common cause of progressive neurological disability in working age persons. However, there is significant inter-individual heterogeneity in disease activity and response to treatment. Currently, the ability to predict at diagnosis who will have a benign, intermediate, or aggressive disease course is very limited. There is therefore a need for integrated predictive tools to inform individualised treatment decision-making. FutureMS is a nationally representative, prospective observation cohort study comprising of 440 participants with a new diagnosis of relapsing remitting MS living in Scotland between May 2016 and March 2019. Established with the aim of addressing this need for individualised predictive tools, the cohort is designed to combine detailed clinical phenotyping with imaging, genetic and biomarker metrics of disease activity and progression. Recruitment, baseline assessment and follow up at year one is complete and longer term follow up is planned, beginning at five years after first visit. The study aims to explore the pathobiology and determinants of disease heterogeneity in MS. Here we describe the cohort design and present a profile of the participants at baseline and one year of follow up.

Published
2021

3. FutureMS Cohort Profile: A Scottish Multi-Centre Inception Cohort Study of Relapsing-Remitting Multiple Sclerosis

Author

Kearns, P.K.A., primary, Martin, S.J., additional, Chang, J., additional, Meijboom, R., additional, York, E.N., additional, Chen, Y., additional, Weaver, C., additional, Stenson, A., additional, Hafezi, K., additional, Thomson, S., additional, Freyer, E., additional, Murphy, L., additional, Harroud, A., additional, Foley, P., additional, Hunt, D., additional, McLeod, M., additional, O’Riordan, J., additional, Carod-Artal, F.J., additional, MacDougall, N.J.J., additional, Baranzini, S.E., additional, Waldman, A.D., additional, Connick, P., additional, and Chandran, S., additional

Published
2021
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4. Report of the A.O.C.S. refining committee 1942–1943

Author

Mitchell, H. S., Milner, R. T., Barrow, E. R., Cluff, C. B., Crapple, G. A., Durkee, M. M., Fash, R. H., Freyer, E. B., Gudheim, A. R., Kiess, Arthur, Kishlar, Lamar, Kruse, N. F., Law, T. C., Moore, H. E., Spielman, L. A., Sternberg, B. L., and Taylor, W. L.

Published
1943
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5. Report of Seed and Meal Analysis Committee, 1947–48

Author

Brown, L. R., Gerhart, Leonard, Smith, T. C., Dippold, M. W., Anderson, R. E., Dippold, M. W., Earle, F. E., Freyer, E. B., Geddes, W. F., Gunther, J. K., Mehlenbacher, V. C., Brown, L. R., Gunther, J. K., Laing, M. L., Brown, L. R., Mehlenbacher, V. C., Earle, F. R., Potts, T. J., Pohle, W. D., Collins, R. I., Gunther, J. K., Geddes, W. F., Mehlenbacher, V. C., Brown, L. R., Potts, T. J., Anderson, R. E., Ainslie, E. C., Cox, C. H., Potts, T. J., Conner Henry, G., law, T. C., Andrews, R. S., Worthen Agee, G., Caldwell, Brice L., Campbell, Charles Russel, Connor Henry, G., Pack, Frank C., McKinney, R. S., Ainslie, E. C., Anderson, R. E., Brown, L. R., Collins, F. I., cox, C. H., Freyer, Egbert, Kruse, N. F., Law, T. C., McKinney, R. S., Mehlenbacher, V. C., Potts, T. J., Rettger, T. L., and Hopper, T. H.

Published
1948
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6. Report of the refining committee 1944–45

Author

Mitchell, H. S., Milner, R. T., Barrow, E. R., Cluff, C. B., Crapple, G. A., Durkee, M. M., Fash, R. H., Freyer, E. B., James, E. M., Kiess, A., King, R. R., Kishlar, Lamar, Kruse, N. F., Law, T. C., Moore, H. E., Spielman, L. A., Sorensen, S. O., and Maxwell, W. T.

Published
1945
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7. Report of the refining committee—1941–1942

Author

Barrow, E. R., Cluff, C. B., Coffey, C. A., Durkee, M. M., Crapple, G. A., Fash, R. H., Freyer, E. B., Gudheim, A. R., Kiess, Arthur, Kishlar, Lamar, Kruse, N. F., Law, T. C., Moore, H. E., Spielman, L. A., Sternberg, B. L., Taylor, W. L., Wheeler, D. H., and Mitchell, D. S.

Published
1941
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9. Report of the refining committee 1940–41

Author

Barrow, E. R., Cluff, C. B., Coffey, C. A., Durkee, M. M., Fash, R. H., Freyer, E. B., Gudheim, A. R., Kiess, Arthur, Kishlar, Lamar, Kruse, N. F., Law, T. C., Moore, H. E., Spielman, L. A., Sternberg, B. L., Taylor, W. L., and Wheeler, D. H.

Published
1941
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10. Report of the refining committee—1941–1942

Author

Barrow, E. R., Cluff, C. B., Coffey, C. A., Durkee, M. M., Crapple, G. A., Fash, R. H., Freyer, E. B., Gudheim, A. R., Kiess, Arthur, Kishlar, Lamar, Kruse, N. F., Law, T. C., Moore, H. E., Spielman, L. A., Sternberg, B. L., Taylor, W. L., Wheeler, D. H., and Mitchell, H. S.

Published
1942
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12. Report of Seed and Meal Analysis Committee

Author

Boulware, M. G., Cox, C. H., Fix, W. A., Haire, R. R., Pope, R. C., Simth, Chas A., Wilkins, O. C., Rettger, T. L., Conner Henry, G., Ainslie, E. C., Cox, C. H., Potts, T. J., Law, T. C., Ainslie, E. C., Anderson, R. E., Cox, C. H., Freyer, E. B., Law, T. C., MoKinney, R. S., Mehlenbacher, V. C., Milner, R. T., Potts, T. J., Rettger, T. L., and Hopper, T. H.

Published
1947
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15. Report of the Seed and Meal Analysis Committee, 1950–1951

Author

Law, T. C., Cretien, Paul D., Hartwig, M. L., Brown, L. R., Anderson, R. E., Dippold, M. W., Hopper, T. H., Ainslie, E. C., Brown, L. R., McKinney, R. S., Cox, C. H., Mehlenbacher, V. C., Earle, F. R., Potts, T. J., Freyer, E. B., Rettger, T. L., Konen, J. C., and Smith, T. C.

Published
1951
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16. Report of the refining committee 1945–1946

Author

Mitohell, H. S., Milner, R. T., Barrow, E. R., Crapple, G. A., Durkee, M. M., Fash, R. H., Freyer, E. B., James, E. M., Kiess, A., King, R. R., Kishlar, Lamar, Kruse, N. F., Law, T. C., Moore, H. E., Sanders, J. H., Spielman, L. A., Sorensen, S. O., and Maxwell, W. T.

Published
1946
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21. Report of the refining committee 1939–40

Author

Clutt, C. B., Barrow, E. R., Kiess, A. A., Coffey, C. A., Low, T. C., Spielman, L. A., Taylor, W. L., Durkee, M. M., Moor, H. E., Kishlar, L., Kruse, N. F., Wheeler, D. H., Sternberg, B. L., Freyer, E. B., Gudheim, A. R., and Mitchell, H. S.

Published
1940
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25. Report of seed and meal analysis committee May, 1946

Author

Haire, Russell R., Hoffpauir, C. L., McIsaac, D. P., Pope, R. C., Wilkins, O. C., Rettger, T. L., Ainslie, E. C., Cox, C. H., Freyer, E. B., Hayward, J. W., Law, T. C., Mehlenbacher, V. C., McKinney, R. S., Milner, R. T., Potts, T. C., Sorensen, S. O., and Hopper, T. H.

Published
1946
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47. CXCR6 + CD69 + CD8 + T cells in ascites are associated with disease severity in patients with cirrhosis.

Author

Niehaus C, Klein S, Strunz B, Freyer E, Maasoumy B, Wedemeyer H, Björkström NK, Kraft ARM, and Cornberg M

Abstract

Background & Aims: Patients with advanced cirrhosis often develop hepatic decompensation, which is accompanied by systemic inflammation and may eventually lead to acute-on-chronic liver failure. One important cause of systemic hyperinflammation is a dysregulated overshooting immune response in ascites in the abdominal cavity. In this study, we analyzed the role of CD8 + T cells in the ascites immune compartment., Methods: Peripheral blood and ascites fluid were collected from 50 patients with decompensated cirrhosis. Phenotype and functional responses of CD8 + T cells were analyzed, and obtained data were compared with each other as well as with healthy controls and patients with compensated cirrhosis., Results: High-dimensional flow cytometry revealed that CD8 + T cells are abundant in the ascites of patients with cirrhosis and exhibit a chronically activated bystander phenotype with innate-like functions. Indeed, we identified distinct CXCR6 + CD69 + clusters of late effector memory CD8 + T cells that were rarely found in blood and correlated with clinical parameters of disease severity. Moreover, this CD8 + T-cell population was hyperresponsive to innate cytokines and exhibited cytokine-mediated bystander activation. Interestingly, the Janus kinase (JAK) inhibitor tofacitinib was able to effectively block bystander-activated CXCR6 + CD69 + CD8 + T cells and significantly suppress effector molecule production., Conclusions: The results indicate that CXCR6 + CD69 + CD8 + T cells in ascites are associated with disease severity and may contribute to inflammation in patients with decompensated cirrhosis, suggesting that targeted inhibition of this immune cell subset may be a viable therapeutic option., Impact and Implications: Patients with advanced cirrhosis often develop hepatic decompensation, which is accompanied by systemic inflammation and eventually leads to acute-on-chronic liver failure. One important cause of systemic hyperinflammation is a dysregulated overshooting immune response in ascites in the abdominal cavity. In this study, we demonstrate that CXCR6 + CD69 + CD8 + T cells are abundant in the ascites of patients with cirrhosis, exhibit a chronically activated bystander phenotype, and correlate with clinical parameters of disease severity. Moreover, we show that the Janus kinase (JAK) inhibitor tofacitinib can effectively block these bystander-activated CXCR6 + CD69 + CD8 + T cells, suggesting that targeted inhibition of this immune cell subset may be a potential therapeutic strategy., Clinical Trial Number: Prospective registry: INFEKTA (DRKS00010664)., Competing Interests: All authors declare no conflicts of interest related to this work. Please refer to the accompanying ICMJE disclosure forms for further details., (© 2024 The Authors.)

Published
2024
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48. Toll-like receptor 2 orchestrates a tumor suppressor response in non-small cell lung cancer.

Author

Millar FR, Pennycuick A, Muir M, Quintanilla A, Hari P, Freyer E, Gautier P, Meynert A, Grimes G, Coll CS, Zdral S, Victorelli S, Teixeira VH, Connelly J, Passos JF, Ros MA, Wallace WAH, Frame MC, Sims AH, Boulter L, Janes SM, Wilkinson S, and Acosta JC

Subjects
Mice, Animals, Humans, Toll-Like Receptor 2 genetics, Toll-Like Receptor 2 metabolism, Genes, Tumor Suppressor, Lung metabolism, Cellular Senescence genetics, Carcinoma, Non-Small-Cell Lung genetics, Lung Neoplasms genetics
Abstract

Targeting early-stage lung cancer is vital to improve survival. However, the mechanisms and components of the early tumor suppressor response in lung cancer are not well understood. In this report, we study the role of Toll-like receptor 2 (TLR2), a regulator of oncogene-induced senescence, which is a key tumor suppressor response in premalignancy. Using human lung cancer samples and genetically engineered mouse models, we show that TLR2 is active early in lung tumorigenesis, where it correlates with improved survival and clinical regression. Mechanistically, TLR2 impairs early lung cancer progression via activation of cell intrinsic cell cycle arrest pathways and the proinflammatory senescence-associated secretory phenotype (SASP). The SASP regulates non-cell autonomous anti-tumor responses, such as immune surveillance of premalignant cells, and we observe impaired myeloid cell recruitment to lung tumors after Tlr2 loss. Last, we show that administration of a TLR2 agonist reduces lung tumor growth, highlighting TLR2 as a possible therapeutic target., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Published
2022
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49. FutureMS cohort profile: a Scottish multicentre inception cohort study of relapsing-remitting multiple sclerosis.

Author

Kearns PKA, Martin SJ, Chang J, Meijboom R, York EN, Chen Y, Weaver C, Stenson A, Hafezi K, Thomson S, Freyer E, Murphy L, Harroud A, Foley P, Hunt D, McLeod M, O'Riordan J, Carod-Artal FJ, MacDougall NJJ, Baranzini SE, Waldman AD, Connick P, and Chandran S

Subjects
Adult, Biomarkers, Cohort Studies, Disease Progression, Humans, Prospective Studies, Multiple Sclerosis diagnosis, Multiple Sclerosis, Relapsing-Remitting diagnosis, Multiple Sclerosis, Relapsing-Remitting drug therapy
Abstract

Purpose: Multiple sclerosis (MS) is an immune-mediated, neuroinflammatory disease of the central nervous system and in industrialised countries is the most common cause of progressive neurological disability in working age persons. While treatable, there is substantial interindividual heterogeneity in disease activity and response to treatment. Currently, the ability to predict at diagnosis who will have a benign, intermediate or aggressive disease course is very limited. There is, therefore, a need for integrated predictive tools to inform individualised treatment decision making., Participants: Established with the aim of addressing this need for individualised predictive tools, FutureMS is a nationally representative, prospective observational cohort study of 440 adults with a new diagnosis of relapsing-remitting MS living in Scotland at the time of diagnosis between May 2016 and March 2019., Findings to Date: The study aims to explore the pathobiology and determinants of disease heterogeneity in MS and combines detailed clinical phenotyping with imaging, genetic and biomarker metrics of disease activity and progression. Recruitment, baseline assessment and follow-up at year 1 is complete. Here, we describe the cohort design and present a profile of the participants at baseline and 1 year of follow-up., Future Plans: A third follow-up wave for the cohort has recently begun at 5 years after first visit and a further wave of follow-up is funded for year 10. Longer-term follow-up is anticipated thereafter., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY. Published by BMJ.)

Published
2022
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50. Embryonic mesothelial-derived hepatic lineage of quiescent and heterogenous scar-orchestrating cells defined but suppressed by WT1.

Author

Kendall TJ, Duff CM, Boulter L, Wilson DH, Freyer E, Aitken S, Forbes SJ, Iredale JP, and Hastie ND

Subjects
Animals, Cell Lineage, Cicatrix metabolism, Hepatic Stellate Cells metabolism, Liver Cirrhosis metabolism, Mice, Myofibroblasts metabolism, WT1 Proteins metabolism, Cicatrix genetics, Epithelium embryology, Hepatic Stellate Cells cytology, Liver embryology, Liver Cirrhosis genetics, Myofibroblasts cytology, WT1 Proteins genetics
Abstract

Activated hepatic stellate cells (aHSCs) orchestrate scarring during liver injury, with putative quiescent precursor mesodermal derivation. Here we use lineage-tracing from development, through adult homoeostasis, to fibrosis, to define morphologically and transcriptionally discreet subpopulations of aHSCs by expression of WT1, a transcription factor controlling morphological transitions in organogenesis and adult homoeostasis. Two distinct populations of aHSCs express WT1 after injury, and both re-engage a transcriptional signature reflecting embryonic mesothelial origin of their discreet quiescent adult precursor. WT1-deletion enhances fibrogenesis after injury, through upregulated Wnt-signalling and modulation of genes central to matrix persistence in aHSCs, and augmentation of myofibroblastic transition. The mesothelial-derived lineage demonstrates punctuated phenotypic plasticity through bidirectional mesothelial-mesenchymal transitions. Our findings demonstrate functional heterogeneity of adult scar-orchestrating cells that can be whole-life traced back through specific quiescent adult precursors to differential origin in development, and define WT1 as a paradoxical regulator of aHSCs induced by injury but suppressing scarring.

Published
2019
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