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Milatuzumab (hLL1) is a humanised IgG1κ antibody that reacts with a cell surface epitope of human CD74, the human leukocyte antigen (HLA) class-II associated invariant chain present on antigen-presenting cells (APCs), including B cells and dendritic cells.1 Although initially studied for oncologic malignancies,2–5 dysregulation of APCs may also occur in non-malignant disorders, and several preclinical studies showed that milatuzumab modestly inhibited B cell proliferation, enhanced spontaneous migration, alterations of adhesion molecule expression and chemotaxis important for lymphocyte recruitment,6 and also reduced production of interferon-α in stimulated peripheral blood mononuclear cells isolated from healthy donors and patients with systemic lupus erythematosus (SLE) (unpublished results). Migration inhibitory factor (MIF) is a cytokine that activates a multicomponent receptor comprising the CD74 ligand-binding …
Handling editor Josef S Smolen
Contributors All authors were involved with the design, writing, analysis and collection of data.
Funding DJW research was supported by Immunomedics, Inc. DJW and DMG were employed at Immunomedics, Inc., when this study was conducted and owned stock in the company. DMG was founder and former Chairman and Chief Scientific Officer, and the inventor or co-inventor on several patents covering milatuzumab.
Competing interests None declared.
Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.
Patient consent for publication Not required.
Provenance and peer review Not commissioned; externally peer reviewed.
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