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A correction to this article has been published: Wilson and Butcher, J. Exp. Med. 200 (8) 1091
Published 20 September 2004. doi:10.1084/jem.20041069
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 200, Number 6, 805-809
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Brief Definitive Report

 CCL28 Controls Immunoglobulin (Ig)A Plasma Cell Accumulation in the Lactating Mammary Gland and IgA Antibody Transfer to the Neonate

Eric Wilsona,b and Eugene C. Butchera,b

a Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305
b Center for Molecular Biology and Medicine, Veterans Affairs Palo Alto Health Care System, Palo Alto, CA 94304

Address correspondence to Eric Wilson at his present address, Dept. of Microbiology and Molecular Biology, Brigham Young University, 773 WIDB, Provo, UT 84602. Phone: (801) 422-4138; Fax: (801) 442-0519; email: er4wilson{at}yahoo.com

The accumulation of immunoglobulin (Ig)A antibody-secreting cells (ASCs) in the lactating mammary gland leads to secretion of antibodies into milk and their passive transfer to the suckling newborn. This transfer of IgA from mother to infant provides transient immune protection against a variety of gastrointestinal pathogens. Here we show that the mucosal epithelial chemokine CCL28 is up-regulated in the mammary gland during lactation and that IgA ASCs from this tissue express CCR10 and migrate to CCL28. In vivo treatment with anti-CCL28 antibody blocks IgA ASC accumulation in the mammary gland, inhibiting IgA antibody secretion into milk and the subsequent appearance of antibody in the gastrointestinal tract of nursing neonates. We propose that CCL28 is a key regulator of IgA ASC accumulation in the mammary gland and thus controls the passive transfer of IgA antibodies from mother to infant.

Key Words: cell trafficking • common mucosal immune system • chemokine • passive immunity • milk


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