Journal
JOURNAL FOR IMMUNOTHERAPY OF CANCER
Volume 9, Issue 12, Pages -Publisher
BMJ PUBLISHING GROUP
DOI: 10.1136/jitc-2021-003585
Keywords
cytokines; immunotherapy; antibodies; neoplasm; biomarkers; tumor; autoimmunity
Categories
Funding
- National Cancer Institute Midcareer Investigator Award in Patient-Oriented Research [K24 CA201543-01]
- National Institute of Allergy and Infectious Disease [1U01AI156189-01]
- American Cancer Society-Melanoma Research Alliance Team Award [MRAT-18-114-01-LIB]
- V Foundation Robin Roberts Cancer Survivorship Award [DT2019-007]
- University of Texas Lung Cancer Specialized Program of Research Excellence [P50CA070907-21]
- UT Southwestern Burroughs Wellcome Fund Physician-Scientist Institutional Award
- Human Genomics/Microarray Core at the Harold C. Simmons Comprehensive Cancer Center [2P30 CA142543-01]
- Biomarker Research Core at the Harold C. Simmons Comprehensive Cancer Center [2P30 CA142543-01]
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This case study demonstrates the potential for late-onset changes in humoral and cellular immunity in patients receiving ICI treatment. Corticosteroid administration resulted in immediate and profound decreases in cytokines, autoantibodies, and inflammatory cells, highlighting the biological effects of corticosteroids on these parameters. Application of humoral and cellular immune biomarkers across ICI populations may inform toxicity monitoring and management.
Immune-related adverse events (irAE) may affect almost any organ system and occur at any point during treatment with immune checkpoint inhibitors (ICI). We present a patient with advanced lung cancer receiving antiprogrammed death 1 checkpoint inhibitor who developed a delayed-onset visual irAE treated with corticosteroids. Through assessment of longitudinal biospecimens, we analyzed serial autoantibodies, cytokines, and cellular populations. Months after ICI initiation and preceding clinical toxicity, the patient developed broad increases in cytokines (most notably interleukin-6 (IL-6), interferon-gamma (IFN gamma), C-X-C motif chemokine ligand 2 (CXCL2), and C-C motif chemokine ligand 17 (CCL17)), autoantibodies (including anti-angiotensin receptor, alpha-actin, and amyloid), CD8 T cells, and plasmablasts. Such changes were not observed in healthy controls and ICI-treated patients without irAE. Administration of corticosteroids resulted in immediate and profound decreases in cytokines, autoantibodies, and inflammatory cells. This case highlights the potential for late-onset changes in humoral and cellular immunity in patients receiving ICI. It also demonstrates the biologic effects of corticosteroids on these parameters. Application of humoral and cellular immune biomarkers across ICI populations may inform toxicity monitoring and management.
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