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Splenectomy Delays Uterine Natural Killer Cell Recruitment to Implantation Sites and Prolongs Pregnancy in Mice
Author(s) -
Zavan Bruno,
Carvalho Celiane Cardoso,
Rossi Wagner Costa,
Paffaro AndrÉa Mollica Amarante,
Paffaro Valdemar Antonio
Publication year - 2012
Publication title -
the anatomical record: advances in integrative anatomy and evolutionary biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.678
H-Index - 62
eISSN - 1932-8494
pISSN - 1932-8486
DOI - 10.1002/ar.22498
Subject(s) - spleen , biology , decidua , progenitor cell , natural killer cell , decidualization , andrology , immunology , stromal cell , angiogenesis , medicine , placenta , endocrinology , stem cell , uterus , pregnancy , fetus , microbiology and biotechnology , cytotoxic t cell , cancer research , in vitro , biochemistry , genetics
Uterine natural killer (uNK) cells are the dominant lymphocytes found in pregnant mammals that develop uterine decidualization. Four stages of mouse uNK cell differentiation are recognized using Dolichos biflorus agglutinin (DBA) lectin histochemistry. Each uNK cell subtype has a preferential domain. In human and mouse normal pregnancies, uNK cells are activated interferon gamma‐producing cells that promote angiogenesis and development of the decidua and placenta. Murine transplant models suggest that uNK cells differentiate from self‐renewing progenitors found in peripheral secondary lymphoid tissues, particularly spleen and lymph nodes. In this work, the spleen was removed 7 days before mice were mated to address whether absence of the spleen reduced uNK cell numbers or altered the distributions of maturing uNK cell subsets using quantitative lectin histochemistry. Splenectomy delayed uNK cell maturation within implantation sites. This coincided with delayed decidual and placental development and a significant (48 hr) lengthening of gestation without loss of viability. These studies characterize spleen as a biologically important progenitor tissue for uNK precursor cells. Anat Rec, 2012. © 2012 Wiley Periodicals, Inc.