Immune checkpoint inhibitor-induced neurotoxicity is not associated with seroprevalence of neurotropic infections.


Journal

Cancer immunology, immunotherapy : CII
ISSN: 1432-0851
Titre abrégé: Cancer Immunol Immunother
Pays: Germany
ID NLM: 8605732

Informations de publication

Date de publication:
Nov 2023
Historique:
received: 22 05 2023
accepted: 07 07 2023
medline: 23 10 2023
pubmed: 22 8 2023
entrez: 22 8 2023
Statut: ppublish

Résumé

Immune checkpoint inhibitors (ICI) substantially improve outcome for patients with cancer. However, the majority of patients develops immune-related adverse events (irAEs), which can be persistent and significantly reduce quality of life. Neurological irAEs occur in 1-5% of patients and can induce severe, permanent sequelae or even be fatal. In order to improve the diagnosis and treatment of neurological irAEs and to better understand their pathogenesis, we assessed whether previous neurotropic infections are associated with neurological irAEs. Neurotropic infections that might predispose to ICI-induced neurological irAEs were analyzed in 61 melanoma patients from 3 countries, the Netherlands, Australia and Germany, including 24 patients with neurotoxicity and 37 control patients. In total, 14 viral, 6 bacterial, and 1 protozoal infections previously reported to trigger neurological pathologies were assessed using routine serology testing. The Dutch and Australian cohorts (NL) included pre-treatment plasma samples of patients treated with neoadjuvant ICI therapy (OpACIN-neo and PRADO trials; NCT02977052). In the Dutch/Australian cohort a total of 11 patients with neurological irAEs were compared to 27 control patients (patients without neurological irAEs). The German cohort (LMU) consisted of serum samples of 13 patients with neurological irAE and 10 control patients without any documented irAE under ICI therapy. The association of neurological irAEs with 21 possible preceding infections was assessed by measuring specific antibodies against investigated agents. The seroprevalence of all the tested viral (cytomegalovirus, Epstein-Barr-Virus, varicella-zoster virus, measles, rubella, influenza A and B, human herpes virus 6 and 7, herpes simplex virus 1 and 2, parvovirus B19, hepatitis A and E and human T-lymphotropic virus type 1 and 2), bacterial (Borrelia burgdorferi sensu lato, Campylobacter jejuni, Mycoplasma pneumoniae, Coxiella burnetti, Helicobacter pylori, Yersinia enterocolitica and Y. pseudotuberculosis) and protozoal (Toxoplasma gondii) infections was similar for patients who developed neurological irAEs as compared to control patients. Thus, the analysis provided no evidence for an association of described agents tested for seroprevalence with ICI induced neurotoxicity. Previous viral, bacterial and protozoal neurotropic infections appear not to be associated with the development of neurological irAEs in melanoma patients who underwent therapy with ICI across 3 countries. Further efforts are needed to unravel the factors underlying neurological irAEs in order to identify risk factors for these toxicities, especially with the increasing use of ICI in earlier stage disease.

Sections du résumé

BACKGROUND BACKGROUND
Immune checkpoint inhibitors (ICI) substantially improve outcome for patients with cancer. However, the majority of patients develops immune-related adverse events (irAEs), which can be persistent and significantly reduce quality of life. Neurological irAEs occur in 1-5% of patients and can induce severe, permanent sequelae or even be fatal. In order to improve the diagnosis and treatment of neurological irAEs and to better understand their pathogenesis, we assessed whether previous neurotropic infections are associated with neurological irAEs.
METHODS METHODS
Neurotropic infections that might predispose to ICI-induced neurological irAEs were analyzed in 61 melanoma patients from 3 countries, the Netherlands, Australia and Germany, including 24 patients with neurotoxicity and 37 control patients. In total, 14 viral, 6 bacterial, and 1 protozoal infections previously reported to trigger neurological pathologies were assessed using routine serology testing. The Dutch and Australian cohorts (NL) included pre-treatment plasma samples of patients treated with neoadjuvant ICI therapy (OpACIN-neo and PRADO trials; NCT02977052). In the Dutch/Australian cohort a total of 11 patients with neurological irAEs were compared to 27 control patients (patients without neurological irAEs). The German cohort (LMU) consisted of serum samples of 13 patients with neurological irAE and 10 control patients without any documented irAE under ICI therapy.
RESULTS RESULTS
The association of neurological irAEs with 21 possible preceding infections was assessed by measuring specific antibodies against investigated agents. The seroprevalence of all the tested viral (cytomegalovirus, Epstein-Barr-Virus, varicella-zoster virus, measles, rubella, influenza A and B, human herpes virus 6 and 7, herpes simplex virus 1 and 2, parvovirus B19, hepatitis A and E and human T-lymphotropic virus type 1 and 2), bacterial (Borrelia burgdorferi sensu lato, Campylobacter jejuni, Mycoplasma pneumoniae, Coxiella burnetti, Helicobacter pylori, Yersinia enterocolitica and Y. pseudotuberculosis) and protozoal (Toxoplasma gondii) infections was similar for patients who developed neurological irAEs as compared to control patients. Thus, the analysis provided no evidence for an association of described agents tested for seroprevalence with ICI induced neurotoxicity.
CONCLUSION CONCLUSIONS
Previous viral, bacterial and protozoal neurotropic infections appear not to be associated with the development of neurological irAEs in melanoma patients who underwent therapy with ICI across 3 countries. Further efforts are needed to unravel the factors underlying neurological irAEs in order to identify risk factors for these toxicities, especially with the increasing use of ICI in earlier stage disease.

Identifiants

pubmed: 37606856
doi: 10.1007/s00262-023-03498-0
pii: 10.1007/s00262-023-03498-0
pmc: PMC10576679
doi:

Substances chimiques

Immune Checkpoint Inhibitors 0
Antineoplastic Agents, Immunological 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

3475-3489

Informations de copyright

© 2023. The Author(s).

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Auteurs

C Schmitt (C)

Department of Dermatology and Allergy, University Hospital, LMU Munich, Munich, Germany.

E P Hoefsmit (EP)

Department of Molecular Oncology and Immunology, Netherlands Cancer Institute, Amsterdam, The Netherlands.

T Fangmeier (T)

Department of Dermatology and Allergy, University Hospital, LMU Munich, Munich, Germany.

N Kramer (N)

Department of Dermatology and Allergy, University Hospital, LMU Munich, Munich, Germany.

C Kabakci (C)

Department of Dermatology and Allergy, University Hospital, LMU Munich, Munich, Germany.

J Vera González (J)

Department of Dermatology, Uniklinikum Erlangen and Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Erlangen, Germany.

J M Versluis (JM)

Department of Medical Oncology, Netherlands Cancer Institute, Amsterdam, The Netherlands.

A Compter (A)

Department of Neuro-Oncology, Netherlands Cancer Institute, Amsterdam, The Netherlands.

T Harrer (T)

Department of Internal Medicine 3, Infectious Diseases and Immunodeficiency Section, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
Deutsches Zentrum Für Immuntherapie (DZI), Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, Erlangen, Germany.

H Mijočević (H)

Max Von Pettenkofer Institute of Hygiene and Medical Microbiology, Faculty of Medicine, LMU Munich, Munich, Germany.

S Schubert (S)

Max Von Pettenkofer Institute of Hygiene and Medical Microbiology, Faculty of Medicine, LMU Munich, Munich, Germany.

T Hundsberger (T)

Departments of Neurology and Medical Oncology/Haematology, Cantonal Hospital, St. Gallen, Switzerland.

A M Menzies (AM)

Melanoma Institute of Australia, The University of Sydney, Sydney, NSW, Australia.
Faculty of Medicine and Health, The University of Sydney, Sydney, NSW, Australia.
Department of Medical Oncology, Royal North Shore and Mater Hospitals, Sydney, NSW, Australia.

R A Scolyer (RA)

Melanoma Institute of Australia, The University of Sydney, Sydney, NSW, Australia.
Faculty of Medicine and Health, The University of Sydney, Sydney, NSW, Australia.
Charles Perkins Centre, The University of Sydney, Sydney, NSW, Australia.
Tissue Pathology and Diagnostic Oncology, Royal Prince Alfred Hospital and NSW Health Pathology, Sydney, NSW, Australia.

G V Long (GV)

Melanoma Institute of Australia, The University of Sydney, Sydney, NSW, Australia.
Faculty of Medicine and Health, The University of Sydney, Sydney, NSW, Australia.
Department of Medical Oncology, Royal North Shore and Mater Hospitals, Sydney, NSW, Australia.
Charles Perkins Centre, The University of Sydney, Sydney, NSW, Australia.

L E French (LE)

Department of Dermatology and Allergy, University Hospital, LMU Munich, Munich, Germany.
Dr. Philip Frost, Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL, USA.

C U Blank (CU)

Department of Molecular Oncology and Immunology, Netherlands Cancer Institute, Amsterdam, The Netherlands.
Department of Medical Oncology, Netherlands Cancer Institute, Amsterdam, The Netherlands.
Department of Medical Oncology, Leiden University Medical Center, Leiden, The Netherlands.

L M Heinzerling (LM)

Department of Dermatology and Allergy, University Hospital, LMU Munich, Munich, Germany. Lucie.Heinzerling@med.uni-muenchen.de.
Department of Dermatology, Uniklinikum Erlangen and Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Erlangen, Germany. Lucie.Heinzerling@med.uni-muenchen.de.

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