Keratinocyte growth factor impairs human thymic recovery from lymphopenia

The lymphocyte-depleting antibody alemtuzumab is a highly effective treatment of relapsing-remitting multiple sclerosis (RRMS); however 50% of patients develop novel autoimmunity post-treatment. Most at risk are individuals who reconstitute their T-cell pool by proliferating residual cells, rather t...

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Published in:JCI insight Vol. 4; no. 12
Main Authors: Coles, Alasdair J., Azzopardi, Laura, Kousin-Ezewu, Onajite, Mullay, Harpreet Kaur, Thompson, Sara A.J., Jarvis, Lorna, Davies, Jessica, Howlett, Sarah, Rainbow, Daniel, Babar, Judith, Sadler, Timothy J., Brown, J. William L., Needham, Edward, May, Karen, Georgieva, Zoya G., Handel, Adam E., Maio, Stefano, Deadman, Mary, Rota, Ioanna, Holländer, Georg, Dawson, Sarah, Jayne, David, Seggewiss-Bernhardt, Ruth, Douek, Daniel C., Isaacs, John D., Jones, Joanne L.
Format: Journal Article
Language:English
Published: United States American Society for Clinical Investigation 20.06.2019
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ISSN:2379-3708, 2379-3708
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Abstract The lymphocyte-depleting antibody alemtuzumab is a highly effective treatment of relapsing-remitting multiple sclerosis (RRMS); however 50% of patients develop novel autoimmunity post-treatment. Most at risk are individuals who reconstitute their T-cell pool by proliferating residual cells, rather than producing new T-cells in the thymus; raising the possibility that autoimmunity might be prevented by increasing thymopoiesis. Keratinocyte growth factor (palifermin) promotes thymopoiesis in non-human primates. Following a dose-tolerability sub-study, individuals with RRMS (duration ≤10 years; expanded disability status scale ≤5·0; with ≥2 relapses in the previous 2 years) were randomised to placebo or 180mcg/kg/day palifermin, given for 3 days immediately prior to and after each cycle of alemtuzumab, with repeat doses at M1 and M3. The interim primary endpoint was naïve CD4+ T-cell count at M6. Exploratory endpoints included: number of recent thymic-emigrants (RTEs) and signal-joint T-cell receptor excision circles (sjTRECs)/mL of blood. The trial primary endpoint was incidence of autoimmunity at M30. At M6, individuals receiving palifermin had fewer naïve CD4+T-cells (2.229x107/L vs. 7.733x107/L; p=0.007), RTEs (16% vs. 34%) and sjTRECs/mL (1100 vs. 3396), leading to protocol-defined termination of recruitment. No difference was observed in the rate of autoimmunity between the two groupsConclusion: In contrast to animal studies, palifermin reduced thymopoiesis in our patients. These results offer a note of caution to those using palifermin to promote thymopoiesis in other settings, particularly in the oncology/haematology setting where alemtuzumab is often used as part of the conditioning regime. ClinicalTrials.gov NCT01712945Funding: MRC and Moulton Charitable Foundation.
AbstractList The lymphocyte-depleting antibody alemtuzumab is a highly effective treatment of relapsing-remitting multiple sclerosis (RRMS); however 50% of patients develop novel autoimmunity post-treatment. Most at risk are individuals who reconstitute their T-cell pool by proliferating residual cells, rather than producing new T-cells in the thymus; raising the possibility that autoimmunity might be prevented by increasing thymopoiesis. Keratinocyte growth factor (palifermin) promotes thymopoiesis in non-human primates. Following a dose-tolerability sub-study, individuals with RRMS (duration ≤10 years; expanded disability status scale ≤5·0; with ≥2 relapses in the previous 2 years) were randomised to placebo or 180mcg/kg/day palifermin, given for 3 days immediately prior to and after each cycle of alemtuzumab, with repeat doses at M1 and M3. The interim primary endpoint was naïve CD4+ T-cell count at M6. Exploratory endpoints included: number of recent thymic-emigrants (RTEs) and signal-joint T-cell receptor excision circles (sjTRECs)/mL of blood. The trial primary endpoint was incidence of autoimmunity at M30. At M6, individuals receiving palifermin had fewer naïve CD4+T-cells (2.229x107/L vs. 7.733x107/L; p=0.007), RTEs (16% vs. 34%) and sjTRECs/mL (1100 vs. 3396), leading to protocol-defined termination of recruitment. No difference was observed in the rate of autoimmunity between the two groupsConclusion: In contrast to animal studies, palifermin reduced thymopoiesis in our patients. These results offer a note of caution to those using palifermin to promote thymopoiesis in other settings, particularly in the oncology/haematology setting where alemtuzumab is often used as part of the conditioning regime. ClinicalTrials.gov NCT01712945Funding: MRC and Moulton Charitable Foundation.
The lymphocyte-depleting antibody alemtuzumab is a highly effective treatment of relapsing-remitting multiple sclerosis (RRMS); however 50% of patients develop novel autoimmunity post-treatment. Most at risk are individuals who reconstitute their T-cell pool by proliferating residual cells, rather than producing new T-cells in the thymus; raising the possibility that autoimmunity might be prevented by increasing thymopoiesis. Keratinocyte growth factor (palifermin) promotes thymopoiesis in non-human primates.BACKGROUNDThe lymphocyte-depleting antibody alemtuzumab is a highly effective treatment of relapsing-remitting multiple sclerosis (RRMS); however 50% of patients develop novel autoimmunity post-treatment. Most at risk are individuals who reconstitute their T-cell pool by proliferating residual cells, rather than producing new T-cells in the thymus; raising the possibility that autoimmunity might be prevented by increasing thymopoiesis. Keratinocyte growth factor (palifermin) promotes thymopoiesis in non-human primates.Following a dose-tolerability sub-study, individuals with RRMS (duration ≤10 years; expanded disability status scale ≤5·0; with ≥2 relapses in the previous 2 years) were randomised to placebo or 180mcg/kg/day palifermin, given for 3 days immediately prior to and after each cycle of alemtuzumab, with repeat doses at M1 and M3. The interim primary endpoint was naïve CD4+ T-cell count at M6. Exploratory endpoints included: number of recent thymic-emigrants (RTEs) and signal-joint T-cell receptor excision circles (sjTRECs)/mL of blood. The trial primary endpoint was incidence of autoimmunity at M30.METHODSFollowing a dose-tolerability sub-study, individuals with RRMS (duration ≤10 years; expanded disability status scale ≤5·0; with ≥2 relapses in the previous 2 years) were randomised to placebo or 180mcg/kg/day palifermin, given for 3 days immediately prior to and after each cycle of alemtuzumab, with repeat doses at M1 and M3. The interim primary endpoint was naïve CD4+ T-cell count at M6. Exploratory endpoints included: number of recent thymic-emigrants (RTEs) and signal-joint T-cell receptor excision circles (sjTRECs)/mL of blood. The trial primary endpoint was incidence of autoimmunity at M30.At M6, individuals receiving palifermin had fewer naïve CD4+T-cells (2.229x107/L vs. 7.733x107/L; p=0.007), RTEs (16% vs. 34%) and sjTRECs/mL (1100 vs. 3396), leading to protocol-defined termination of recruitment. No difference was observed in the rate of autoimmunity between the two groupsConclusion: In contrast to animal studies, palifermin reduced thymopoiesis in our patients. These results offer a note of caution to those using palifermin to promote thymopoiesis in other settings, particularly in the oncology/haematology setting where alemtuzumab is often used as part of the conditioning regime.FINDINGSAt M6, individuals receiving palifermin had fewer naïve CD4+T-cells (2.229x107/L vs. 7.733x107/L; p=0.007), RTEs (16% vs. 34%) and sjTRECs/mL (1100 vs. 3396), leading to protocol-defined termination of recruitment. No difference was observed in the rate of autoimmunity between the two groupsConclusion: In contrast to animal studies, palifermin reduced thymopoiesis in our patients. These results offer a note of caution to those using palifermin to promote thymopoiesis in other settings, particularly in the oncology/haematology setting where alemtuzumab is often used as part of the conditioning regime.ClinicalTrials.gov NCT01712945Funding: MRC and Moulton Charitable Foundation.TRIAL REGISTRATIONClinicalTrials.gov NCT01712945Funding: MRC and Moulton Charitable Foundation.
Keratinocyte growth factor impairs T cell recovery in patients with relapsing-remitting multiple sclerosis receiving treatment with the lymphocyte-depleting monoclonal antibody alemtuzumab.
Author Douek, Daniel C.
Jones, Joanne L.
Handel, Adam E.
Sadler, Timothy J.
Jayne, David
Holländer, Georg
Needham, Edward
Isaacs, John D.
Kousin-Ezewu, Onajite
Brown, J. William L.
Seggewiss-Bernhardt, Ruth
Dawson, Sarah
Howlett, Sarah
Deadman, Mary
Davies, Jessica
Coles, Alasdair J.
Mullay, Harpreet Kaur
Jarvis, Lorna
May, Karen
Thompson, Sara A.J.
Rainbow, Daniel
Maio, Stefano
Azzopardi, Laura
Rota, Ioanna
Babar, Judith
Georgieva, Zoya G.
AuthorAffiliation 7 Department of Hematology/Oncology, Soziastiftung Bamberg, Bamberg, Germany
2 Nuffield Department of Clinical Neurosciences and
8 National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland, USA
9 Institute of Cellular Medicine, Newcastle University, and Musculoskeletal Unit, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, United Kingdom
6 University Hospital of Würzburg, Würzburg, Germany
5 Medical Research Council (MRC) Biostatistics Unit, Cambridge Institute of Public Health, Cambridge, United Kingdom
3 Department of Paediatrics, University of Oxford, Oxford, United Kingdom
1 Department of Clinical Neurosciences, University of Cambridge, Cambridge, United Kingdom
4 Cambridge Clinical Trials Unit, Cambridge University Hospitals NHS Foundation Trust, Cambridge, United Kingdom
AuthorAffiliation_xml – name: 3 Department of Paediatrics, University of Oxford, Oxford, United Kingdom
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Issue 12
Keywords T cell development
Immunology
Autoimmune diseases
T cells
Therapeutics
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Snippet The lymphocyte-depleting antibody alemtuzumab is a highly effective treatment of relapsing-remitting multiple sclerosis (RRMS); however 50% of patients develop...
Keratinocyte growth factor impairs T cell recovery in patients with relapsing-remitting multiple sclerosis receiving treatment with the lymphocyte-depleting...
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SubjectTerms Adolescent
Adult
Animals
CD4-Positive T-Lymphocytes - immunology
CD52 Antigen - metabolism
Clinical Medicine
Disease Models, Animal
Female
Fibroblast Growth Factor 7 - pharmacology
Fibroblast Growth Factor 7 - therapeutic use
Humans
Lymphopenia - drug therapy
Male
Mice
Middle Aged
Multiple Sclerosis, Relapsing-Remitting - immunology
Young Adult
Title Keratinocyte growth factor impairs human thymic recovery from lymphopenia
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https://pubmed.ncbi.nlm.nih.gov/PMC6629095
Volume 4
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