Reviews
Checkpoint inhibition-induced sicca: a type II interferonopathy?
S. Pringle1, X. Wang2, A. Vissink3, H. Bootsma4, F.G. Kroese5
- Department of Rheumatology and Clinical Immunology, University Medical Centre Groningen, University of Groningen, The Netherlands. s.a.pringle@umcg.nl
- Department of Rheumatology and Clinical Immunology, University Medical Centre Groningen, University of Groningen, the Netherlands.
- Department of Oral and Maxillofacial Surgery, University Medical Centre Groningen, University of Groningen, The Netherlands.
- Department of Rheumatology and Clinical Immunology, University Medical Centre Groningen, University of Groningen, the Netherlands.
- Department of Rheumatology and Clinical Immunology, University Medical Centre Groningen, University of Groningen, the Netherlands.
CER13755
2020 Vol.38, N°4 ,Suppl.126
PI 0253, PF 0260
Reviews
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PMID: 33025881 [PubMed]
Received: 30/06/2020
Accepted : 27/07/2020
In Press: 22/09/2020
Published: 23/10/2020
Abstract
The advent of immune checkpoint inhibitor (ICI) therapy for treatment of cancers is unfortunately coupled with a broad panoply of side effects, related to non-specific activation of the immune system. One such side effect is the development of sicca complaints. This culminates in a proportion of patients who, according to the ACR-EULAR 2016 criteria, can be classified as suffering from the autoimmune disease primary Sjögren’s syndrome (pSS). Although salivary gland (SG) loss of function is often seen after ICI therapy, the similarities with ‘classical’ pSS patients would appear to end there. Despite the presence of focal lymphocytic sialadenitis typical for SS in salivary gland biopsies from patients receiving ICI therapy, the nature of the immune infiltration (foci) following ICI use (T-cell dominated) is starkly different to that in pSS (B-cell dominated). The SG parenchyma post-ICI use does not present with germinal centres, lymphoepithelial lesions or IgG plasma cells, which are frequently found in the SG in pSS. Here we review the functional deterioration of SGs following ICI use, the SG parenchyma phenotype associated with this, and ultrasound abnormalities. We conclude by suggesting that ICI-induced SG dysfunction may represent a new interferonopathy, driven by IFNγ, and that this ‘pSS’ patient cohort may require a different management than classical pSS patients.
