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Link to original content: https://pubmed.ncbi.nlm.nih.gov/15381732
CCL28 controls immunoglobulin (Ig)A plasma cell accumulation in the lactating mammary gland and IgA antibody transfer to the neonate - PubMed Skip to main page content
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. 2004 Sep 20;200(6):805-9.
doi: 10.1084/jem.20041069.

CCL28 controls immunoglobulin (Ig)A plasma cell accumulation in the lactating mammary gland and IgA antibody transfer to the neonate

Eric Wilson  1 , Eugene C Butcher
Affiliations

CCL28 controls immunoglobulin (Ig)A plasma cell accumulation in the lactating mammary gland and IgA antibody transfer to the neonate

Eric Wilson et al. J Exp Med. .

Erratum in

  • J Exp Med. 2004 Oct 18;200(8):following 1089

Abstract

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.

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Figures

Figure 1.
Figure 1.
CCL28 expression in the mammary gland is up-regulated during lactation. RT-PCR was performed using primers specific for mouse CCL28 and GAPDH using mammary gland total RNA.
Figure 2.
Figure 2.
Mammary gland IgA ASCs migrate to CCL28, bind CCL28–Ig chimera, and express CCR10. Lymphocytes were isolated from the mammary gland and small intestine of lactating mice. (A) Migration of mammary gland and small intestine IgA ASCs to CCL25 (black bars), CCL28 (hatched bars), and CXCL12 (white bars). **, differences were statistically significant (P < 0.01) between CCL28 and CCL25 migration. Data are expressed as mean ± SEM. (B) CCL28–Ig binding. Left, negative control; right, CCL28–Ig binding. (C) Total RNA was collected from sorted mammary gland IgA ASCs. RT-PCR analysis shows expression of the chemokine receptor CCR10 but not CCR3 on mammary gland IgA ASCs.
Figure 3.
Figure 3.
Anti-CCL28 inhibits IgA ASC homing to the mammary gland and IgA antibody accumulation in the milk. (A) Tissue sections from the mammary gland of 9-d postpartum mice treated with anti-CCL28 function-blocking antibody or isotype control antibody. Tissue sections were stained with anti-IgA (green) and anti–TCR-β (red) antibodies. The subiliac lymph node is included in the top region of each photograph as a reference point. A magnification of 200. (B) Milk was collected on days 1 and 9 postpartum from mice treated with anti-CCL28 or isotype control antibody. IgA, IgG1, and IgM levels in the milk were determined. Horizontal bars represent the average of each group. Differences between IgA ASCs and IgA antibody accumulation between control and anti-CCL28 treatment groups were statistically significant (P < 0.001).
Figure 4.
Figure 4.
Anti-CCL28 blockade inhibits passive transfer of maternal IgA to the neonate. Feces were collected from 9-d-old neonates nursing on mothers treated with anti-CCL28 or isotype control antibody, and IgA levels were determined. **, statistically significant difference (P < 0.01). Data are expressed as mean ± SEM.
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