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To B or not to B—that is the question for myocardial infarction

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After myocardial infarction (MI), circulating B cells produce the chemokine Ccl7, which mobilizes inflammatory monocytes from the bone marrow into the blood, after which they are then recruited to the injured heart, a new study shows. B cell depletion after MI limits myocardial injury and improves heart function, suggesting a new approach for the management of acute MI (pages 1273–1280).

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Figure 1: B cells are key sentinels after myocardial infarction.

Katie Vicari

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Authors and Affiliations

  1. Division of Rheumatology, Nancy D. Kim and Andrew D. Luster are at the Center for Immunology & Inflammatory Diseases, Allergy & Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.,

    Nancy D Kim & Andrew D Luster

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  1. Nancy D Kim
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  2. Andrew D Luster
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Correspondence to Andrew D Luster.

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The authors declare no competing financial interests.

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Kim, N., Luster, A. To B or not to B—that is the question for myocardial infarction. Nat Med 19, 1208–1210 (2013). https://doi.org/10.1038/nm.3367

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