Cytokine changes during immune-related adverse events and corticosteroid treatment in melanoma patients receiving immune checkpoint inhibitors.


Journal

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

Informations de publication

Date de publication:
Aug 2021
Historique:
received: 15 09 2020
accepted: 06 01 2021
pubmed: 23 1 2021
medline: 27 7 2021
entrez: 22 1 2021
Statut: ppublish

Résumé

Immune checkpoint inhibitors (ICIs) often cause immune-related adverse events (irAEs), most of which are treated with corticosteroids despite evidence suggesting that corticosteroids may blunt antitumor efficacy. We sought to identify cytokine changes that correlate with irAEs and study the impact of corticosteroid treatment on cytokine levels. We analyzed expression of 34 cytokines in 52 melanoma patients who developed irAEs during therapy with ICIs. Luminex serum assay was performed at baseline, 1, 2, and 3 months after starting ICI. Baseline cytokine levels and longitudinal log There were no differences in baseline cytokine levels between patients who developed grade 1-2 irAEs (N = 28) vs. grade 3-4 irAEs (N = 24). Dermatitis patients (N = 8) had significantly higher baseline Ang-1 (p = 0.006) and CD40L (p = 0.005). Pneumonitis patients (N = 4) had significantly higher baseline IL-17 (p = 0.009). Colitis patients (N = 8) had a trend toward decreased GCSF (p = 0.08). Through Spearman's correlation analysis, patients who developed irAEs without receiving corticosteroids (N = 23) exhibited harmonization of cytokine fold-change, with 0/276 pairwise comparisons demonstrating significant divergence. In contrast, corticosteroid treatment in patients with irAEs (N = 15) altered fold-change to a discordant pattern (42/276 diverged, 15.2%). This discordant cytokine pattern in patients receiving corticosteroids is similar to the cytokine pattern in patients who did not develop irAEs (N = 8) during the longitudinal profiling period (41/276, 14.9%). Baseline levels of certain cytokines correlate with specific irAEs in melanoma patients receiving ICIs. irAEs drive a concordant pattern of cytokine fold-change, which is disrupted by corticosteroid treatment.

Sections du résumé

BACKGROUND BACKGROUND
Immune checkpoint inhibitors (ICIs) often cause immune-related adverse events (irAEs), most of which are treated with corticosteroids despite evidence suggesting that corticosteroids may blunt antitumor efficacy. We sought to identify cytokine changes that correlate with irAEs and study the impact of corticosteroid treatment on cytokine levels.
METHODS METHODS
We analyzed expression of 34 cytokines in 52 melanoma patients who developed irAEs during therapy with ICIs. Luminex serum assay was performed at baseline, 1, 2, and 3 months after starting ICI. Baseline cytokine levels and longitudinal log
RESULTS RESULTS
There were no differences in baseline cytokine levels between patients who developed grade 1-2 irAEs (N = 28) vs. grade 3-4 irAEs (N = 24). Dermatitis patients (N = 8) had significantly higher baseline Ang-1 (p = 0.006) and CD40L (p = 0.005). Pneumonitis patients (N = 4) had significantly higher baseline IL-17 (p = 0.009). Colitis patients (N = 8) had a trend toward decreased GCSF (p = 0.08). Through Spearman's correlation analysis, patients who developed irAEs without receiving corticosteroids (N = 23) exhibited harmonization of cytokine fold-change, with 0/276 pairwise comparisons demonstrating significant divergence. In contrast, corticosteroid treatment in patients with irAEs (N = 15) altered fold-change to a discordant pattern (42/276 diverged, 15.2%). This discordant cytokine pattern in patients receiving corticosteroids is similar to the cytokine pattern in patients who did not develop irAEs (N = 8) during the longitudinal profiling period (41/276, 14.9%).
CONCLUSIONS CONCLUSIONS
Baseline levels of certain cytokines correlate with specific irAEs in melanoma patients receiving ICIs. irAEs drive a concordant pattern of cytokine fold-change, which is disrupted by corticosteroid treatment.

Identifiants

pubmed: 33481042
doi: 10.1007/s00262-021-02855-1
pii: 10.1007/s00262-021-02855-1
doi:

Substances chimiques

Adrenal Cortex Hormones 0
Cytokines 0
Immune Checkpoint Inhibitors 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2209-2221

Subventions

Organisme : Parker Institute for Cancer Immunotherapy
ID : 5812101

Informations de copyright

© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH, DE part of Springer Nature.

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Auteurs

Kevin Tyan (K)

Harvard Medical School, 25 Shattuck Street, Boston, MA, 02115, USA.
Center for Immuno-Oncology, Department of Medical Oncology, Gastrointestinal Cancer Center, Dana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Avenue, Boston, MA, 02215, USA.

Joanna Baginska (J)

Center for Immuno-Oncology, Department of Medical Oncology, Gastrointestinal Cancer Center, Dana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Avenue, Boston, MA, 02215, USA.

Martha Brainard (M)

Center for Immuno-Oncology, Department of Medical Oncology, Gastrointestinal Cancer Center, Dana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Avenue, Boston, MA, 02215, USA.

Anita Giobbie-Hurder (A)

Division of Biostatistics, Department of Data Sciences, Dana-Farber Cancer Institute, Boston, MA, USA.

Mariano Severgnini (M)

Center for Immuno-Oncology, Department of Medical Oncology, Gastrointestinal Cancer Center, Dana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Avenue, Boston, MA, 02215, USA.

Michael Manos (M)

Center for Immuno-Oncology, Department of Medical Oncology, Gastrointestinal Cancer Center, Dana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Avenue, Boston, MA, 02215, USA.

Rizwan Haq (R)

Harvard Medical School, 25 Shattuck Street, Boston, MA, 02115, USA.
Center for Immuno-Oncology, Department of Medical Oncology, Gastrointestinal Cancer Center, Dana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Avenue, Boston, MA, 02215, USA.

Elizabeth I Buchbinder (EI)

Harvard Medical School, 25 Shattuck Street, Boston, MA, 02115, USA.
Center for Immuno-Oncology, Department of Medical Oncology, Gastrointestinal Cancer Center, Dana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Avenue, Boston, MA, 02215, USA.

Patrick A Ott (PA)

Harvard Medical School, 25 Shattuck Street, Boston, MA, 02115, USA.
Center for Immuno-Oncology, Department of Medical Oncology, Gastrointestinal Cancer Center, Dana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Avenue, Boston, MA, 02215, USA.

F Stephen Hodi (FS)

Harvard Medical School, 25 Shattuck Street, Boston, MA, 02115, USA.
Center for Immuno-Oncology, Department of Medical Oncology, Gastrointestinal Cancer Center, Dana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Avenue, Boston, MA, 02215, USA.

Osama E Rahma (OE)

Harvard Medical School, 25 Shattuck Street, Boston, MA, 02115, USA. Osamae_rahma@DFCI.harvard.edu.
Center for Immuno-Oncology, Department of Medical Oncology, Gastrointestinal Cancer Center, Dana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Avenue, Boston, MA, 02215, USA. Osamae_rahma@DFCI.harvard.edu.

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