Complement components in breast milk may enhance the local immune response
in the gut of infants. In this study, we investigated the expression of com
plement genes in the mammary gland and attempted to determine possible regu
latory mechanisms. We have studied the expression of C3, C4, factor B, and
HLA-DR alpha: mRNA by in situ hybridization in gestational mammary gland sp
ecimens and compared these findings to those in breast tissue affected with
an inflammatory process, lactating adenoma or idiopathic gynecomastia. In
normal resting breast, only C4 mRNA was noted in some ductal epithelium. In
gestational mammary gland, there was a diffuse expression of C4, C3, and f
actor B mRNA in the epithelial cells of the acini. A similar pattern of com
plement gene expression was found in localized areas of an infectious infla
mmatory process. In addition, in the inflammatory specimens, there was also
expression of C3 mRNA in infiltrating macrophages (CD 68 positive cells).
In gynecomastia, C4 mRNA was noted in ductal epithelium, and there was a ma
rked increased expression of C3 mRNA in the proliferating epithelium of the
lactating adenoma. HLA-DRa was observed only in macrophages involved in th
e inflammatory response. Our findings, which reflect the hormonal and infla
mmatory events in vivo, provide new insights as to in situ complement gene
expression.