Pituitary Expression of CTLA-4 Mediates Hypophysitis Secondary to Administration of CTLA-4 Blocking Antibody
By Shintaro Iwama, A. de Remigis, M. Callahan, S. Slovin, J. Wolchok, P. Caturegli. Science Translational Medicine, 2014
651 citations recorded by the source corpus.
Subfields: Endocrinology, Diabetes and Metabolism, Immunology, Oncology
View Paper: https://www.semanticscholar.org/paper/a2fa27ed17df8d90060b476375bf7194e4e41b8d
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Citations in the corpus
- Tumour- and class-specific patterns of immune-related adverse events of immune checkpoint inhibitors: a systematic review (2017, background): “Furthermore, tissue-related factors may also contribute to irAE, for example CTLA-4 expression is found in the pituitary accounting for the greater incidence of hypophysitis with CTLA-4 mAbs [64].”
- Toxicities of the anti-PD-1 and anti-PD-L1 immune checkpoint antibodies. (2016, background): “Other immune cells may play a role in the development of irAEs, including B cells that secrete antibodies that may mediate toxicity [16, 17], granulocytes that secrete inflammatory mediators, and cytokines [16, 18].”
- Immune-related adverse events with immune checkpoint blockade: a comprehensive review. (2016, background): “Serum pituitary auto-antibodies could be present [25].”
- Management of toxicities from immunotherapy: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up. (2018, background): “Recently, in a murine model, low-level ectopic RNA and protein expression of CTLA4 on thyrotropin and prolactin secreting cells of the pituitary gland [30] was demonstrated.”
- Management of toxicities from immunotherapy: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up. (2017, background): “Recently, in a murine model, low-level ectopic RNA and protein expression of CTLA4 on thyrotropin and prolactin secreting cells of the pituitary gland [30] was demonstrated.”
- CTLA-4 and PD-1 Pathways (2016, background): “Hypophysitis is reported in about 2% to 4% of patients receiving ipilimumab but in <1% of patients receiving PD-1 inhibitors(51,54,55,69,80); however, this variation in incidence may not be related to differences in immune mechanism of action, but may be explained by ectopic expression of CTLA-4 in ”
- Toxicities of the anti-PD-1 and anti-PD-L1 immune checkpoint antibodies. (2015, background): “Other immune cells may play a role in the development of irAEs, including B cells that secrete antibodies that may mediate toxicity [16, 17], granulocytes that secrete inflammatory mediators, and cytokines [16, 18].”