Cited by 257Immune Cell Function and InteractionMonoclonal and Polyclonal Antibodies ResearchImmunotoxicology and immune responses

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Mechanism of first-dose cytokine-release syndrome by CAMPATH 1-H: involvement of CD16 (FcgammaRIII) and CD11a/CD18 (LFA-1) on NK cells.

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Wing, M G, Moreau, T, Greenwood, J, Smith, R M, Hale, G, Isaacs, J, Waldmann, H, Lachmann, P J, Compston, A·1996·Journal of Clinical Investigation

DOI 10.1172/jci119110PMC PMC507749

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Abstract

The administration of the immunosuppressive humanized monoclonal antibody CAMPATH 1-H, which recognizes CD52 on lymphocytes and monocytes, is associated with a first-dose cytokine-release syndrome involving TNFalpha, IFNgamma, and IL-6 clinically. In vitro models have been used to establish the cellular source and mechanism responsible for cytokine release, demonstrating that cytokine release is isotype dependent, with the rat IgG2b and human IgG1 isotype inducing the highest levels of cytokine release, which was inhibited with antibody to CD16, the low affinity Fc-receptor for IgG (FcgammaR). Cross-linking antibody opsonized CD4 T lymphocytes failed to stimulate TNFalpha release, which together with the observation that TNFalpha release by purified natural killer (NK) cells stimulated by fixed autologous CAMPATH 1-H-opsonized targets was inhibited with anti-CD16, indicates that cytokine release results from ligation of CD16 on the NK cells, rather than Fc-receptor (FcR)-dependent cross-linking of CD52 on the targeted cell. Since the hierarchy of isotypes inducing cytokine release in these cultures matches that seen clinically, we conclude that ligation of CD16 on NK cells is also responsible for cytokine release after injection of CAMPATH 1-H in vivo.

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Authors: Wing, M. G., Moreau, T., Greenwood, J., Smith, R. M., Hale, G., Isaacs, J., Waldmann, H., Lachmann, P. J., & Compston, A.
Affiliations: Medical Research Council (GB)
University of Cambridge (GB)
University of Oxford (GB)
ORCID: Moreau, T
Smith, R M
Hale, G
Isaacs, J
Waldmann, H
Compston, A
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 1996-12-15
Volume: 98
Issue: 12
Pages: 2819-2826
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci119110
PMC: PMC507749
OpenAlex: W2069219892
Cited by: 257
References: 43
Citations by year: 2026: 2 · 2025: 6 · 2024: 8 · 2023: 5 · 2022: 5 · 2021: 11 · 2020: 12 · 2019: 15 · 2018: 11 · 2017: 11 · 2016: 11 · 2015: 7 · 2014: 8 · 2013: 12 · 2012: 8
FWCI: 1.37
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Wellcome Trust
Medical Research Council
Topics: Life Sciences › Immunology and Microbiology › Immunology › Immune Cell Function and Interaction
Life Sciences › Immunology and Microbiology › Immunology › Monoclonal and Polyclonal Antibodies Research
Life Sciences › Immunology and Microbiology › Immunology › Immunotoxicology and immune responses
Keywords: cytokine release syndrome, CD52, natural killer cells, CD16, Fc gamma receptor I, LFA-1, CD11a/CD18, antibody isotypes, TNF-α, interferon-gamma, interleukin-6
MeSH terms: Alemtuzumab, Antibodies, Monoclonal, Antibodies, Neoplasm, Enzyme-Linked Immunosorbent Assay, Humans, Immunoglobulin G, Immunoglobulin M, Interferon-gamma, Killer Cells, Natural, Leukocytes, Tumor Necrosis Factor-alpha, CD4-Positive T-Lymphocytes, Interleukin-6, Cytokines, Receptors, IgG, CD11 Antigens, Antibodies, Monoclonal, Humanized

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Mechanism of first-dose cytokine-release syndrome by CAMPATH 1-H: involvement of CD16 (FcgammaRIII) and CD11a/CD18 (LFA-1) on NK cells.

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