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乳腺中分泌免疫系统的激素诱导

Hormonal induction of the secretory immune system in the mammary gland.

作者信息

Weisz-Carrington P, Roux M E, McWilliams M, Phillips-Quagliata J M, Lamm M E

出版信息

Proc Natl Acad Sci U S A. 1978 Jun;75(6):2928-32. doi: 10.1073/pnas.75.6.2928.

DOI:10.1073/pnas.75.6.2928
PMID:275864
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC392679/
Abstract

The secretory immune system of the mammary gland is undeveloped in virgin mice but becomes active at term and during lactation. This change appears to depend on migration to the mammary gland of precursors of IgA-secreting cells derived from the gut-associated lymphoid tissue, an origin which explains the specificity of milk IgA antibodies for enteric organisms. Because development of the epithelial components of the mammary gland is clearly under hormonal control, we examined the effect of mammotropic hormones on differentiation of the immune elements. Under a combined regimen of progesterone, estrogen, and prolactin, development of the glandular epithelium occurs with concomitant increments in the number of IgA-secreting plasma cells and amount of intraepithelial IgA. These increases appear to be due to enhanced capacity of the gland to attract or retain precursors of IgA plasma cells derived from gut-associated lymphoid tissue. Testosterone, which antagonizes lactation, also antagonizes development of the secretory immune system and decreases cellular trapping in the lactating gland. The ability of the gland to trap IgA immunoblasts is probably contingent upon a hormone-induced increase in receptors.

摘要

乳腺的分泌免疫系统在未生育的小鼠中未发育成熟,但在足月时和哺乳期会变得活跃。这种变化似乎取决于源自肠道相关淋巴组织的分泌IgA细胞前体迁移至乳腺,这一来源解释了乳汁中IgA抗体对肠道微生物的特异性。由于乳腺上皮成分的发育显然受激素控制,我们研究了促乳激素对免疫成分分化的影响。在孕酮、雌激素和催乳素的联合作用下,腺上皮发生发育,同时分泌IgA的浆细胞数量和上皮内IgA量增加。这些增加似乎是由于乳腺吸引或保留源自肠道相关淋巴组织的IgA浆细胞前体的能力增强所致。拮抗泌乳的睾酮也拮抗分泌免疫系统的发育,并减少泌乳期乳腺中的细胞滞留。乳腺捕获IgA免疫母细胞的能力可能取决于激素诱导的受体增加。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e07/392679/86667170212f/pnas00018-0396-f.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e07/392679/322fb194023c/pnas00018-0396-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e07/392679/8e02ecf7b603/pnas00018-0396-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e07/392679/f101ac7d328b/pnas00018-0396-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e07/392679/c8d62fcf0320/pnas00018-0396-d.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e07/392679/25a714f16844/pnas00018-0396-e.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e07/392679/86667170212f/pnas00018-0396-f.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e07/392679/322fb194023c/pnas00018-0396-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e07/392679/8e02ecf7b603/pnas00018-0396-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e07/392679/f101ac7d328b/pnas00018-0396-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e07/392679/c8d62fcf0320/pnas00018-0396-d.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e07/392679/25a714f16844/pnas00018-0396-e.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e07/392679/86667170212f/pnas00018-0396-f.jpg

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