In recent years it has been increasingly appreciated that B cells constitute a significant part of the immune infiltrate of solid tumors (1). In their interesting paper, Zirakzadeh et al. demonstrate that solid tumors and metastatic lymph nodes are enriched for terminally differentiated B cells, i.e., memory B cells and plasmablasts (2). They furthermore provide evidence that these tumor-associated B cells presumably represent tumor Ag-specific B lymphocytes, which have undergone clonal expansion. Our analysis of patients with esophageal cancer confirms the finding of a plasmacytosis in the peripheral blood (Fig. 1A). The accumulation of plasma cells seems to be a general phenomenon in many tumor entities, and is associated with a better prognosis (3, 4). In addition, we found an increase in CD24highCD38high B cells (Fig. 1A), a subset with regulatory capacity (5). Interestingly, while both adenocarcinoma and squamous cell carcinoma of the esophagus had similar percentages of plasmablasts, adenocarcinomas had a higher proportion of CD24highCD38high B cells (Fig. 1B). Because they solely used the Freiburg classification, Zirakzadeh et al. omit regulatory B cell subsets from their analyses. However, recent publications, including our study of local B cell–depletion in mycosis fungoides, demonstrate that targeting of regulatory B cells seems to be a promising therapeutic concept and that balance between regulatory and terminally differentiated B cells might be of importance (6, 7). Therefore, a detailed understanding of the composition of the B cell infiltrate in tumors will be necessary for the application of B cell–targeted therapeutic interventions for the immunotherapy of malignant diseases.
Comment on “Multiplex B Cell Characterization in Blood, Lymph Nodes, and Tumors from Patients with Malignancies”
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Alexander Shimabukuro-Vornhagen, Hans Anton Schlößer, Dirk Ludger Stippel, Sebastian Theurich, Michael von Bergwelt-Baildon; Comment on “Multiplex B Cell Characterization in Blood, Lymph Nodes, and Tumors from Patients with Malignancies”. J Immunol 1 November 2013; 191 (9): 4471. https://doi.org/10.4049/jimmunol.1390052
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