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Updated: Jun 16, 2026

Indirect Immunofluorescence on Frozen Sections of Mouse Mammary Gland
Published on: December 1, 2015
IgA ASC accumulation to the lactating mammary gland is dependent on VCAM-1 and alpha4 integrins
Elizabeth N Low1, Lauren Zagieboylo, Benjamin Martino
1Department of Microbiology and Molecular Biology, Brigham Young University, Provo, UT 84602, USA.
The homing and migration of IgA antibody secreting cells (ASC) to the lactating mammary gland is essential to the passive transfer of immunity from mother to nursing neonate. Antibody secreting cells, located within the lactating mammary gland, produce high levels of antigen-specific IgA antibodies. These antibodies, which are subsequently transferred to the nursing neonate via breast milk, provide passive immune protection against antigens previously encountered by the mother to the nursing infant. The efficient homing and accumulation of lymphocytes is highly dependent on cellular adhesion molecules expressed on the vascular endothelium and their integrin ligands. Vasculature within the lactating mammary gland is known to express several adhesion molecules, including VCAM-1 and MAdCAM-1. However, the role of these molecules in vivo has not been previously described. Here we show that alpha4 integrins and VCAM-1 play essential roles in mediating the accumulation of IgA ASCs to the lactating mammary gland. Conversely, neither MAdCAM-1 nor its major ligand alpha4beta7 are required for efficient IgA ASC accumulation to this tissue.
The homing and migration of IgA antibody secreting cells (ASC) to the lactating mammary gland is essential to the passive transfer of immunity from mother to nursing neonate. Antibody secreting cells, located within the lactating mammary gland, produce high levels of antigen-specific IgA antibodies. These antibodies, which are subsequently transferred to the nursing neonate via breast milk, provide passive immune protection against antigens previously encountered by the mother to the nursing infant. The efficient homing and accumulation of lymphocytes is highly dependent on cellular adhesion molecules expressed on the vascular endothelium and their integrin ligands. Vasculature within the lactating mammary gland is known to express several adhesion molecules, including VCAM-1 and MAdCAM-1. However, the role of these molecules in vivo has not been previously described. Here we show that alpha4 integrins and VCAM-1 play essential roles in mediating the accumulation of IgA ASCs to the lactating mammary gland. Conversely, neither MAdCAM-1 nor its major ligand alpha4beta7 are required for efficient IgA ASC accumulation to this tissue.
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