title: Effect of TIM-3 Blockade on the Immunophenotype and Cytokine Profile of Murine Uterine NK Cells.
abstract: NK cells are the most abundant lymphocyte population in the feto-maternal interface during gestation. The uterine NK cells (uNK) are transient, have a unique immunophenotype and produce a number of cytokines. These cytokines play an important role in establishment and maintenance of vascular remodeling and tolerance associated with successful pregnancy. The uNK cells also express TIM-3 during gestation and blockade of TIM-3 expression results in fetal loss in mice. In this study we determined the effect of TIM-3 blockade on uNK cells. Specifically we observed surface receptor phenotype and cytokine production by uNK cells following TIM-3 blockade. Our results show that TIM-3 plays a role in regulating the uNK cells and contributes to the maintenance of tolerance at the feto-maternal interface.
authors.affiliation: Children's Hospital Boston, Renal Division, Harvard Medical School, Boston, Massachusetts, United States of America.
authors.forename: Sudipta
authors.initials: S
authors.lastname: Tripathi
authors.affiliation: Children's Hospital Boston, Renal Division, Harvard Medical School, Boston, Massachusetts, United States of America.
authors.forename: Lola
authors.initials: L
authors.lastname: Chabtini
authors.affiliation: Children's Hospital Boston, Renal Division, Harvard Medical School, Boston, Massachusetts, United States of America.
authors.forename: Pranal J
authors.initials: PJ
authors.lastname: Dakle
authors.affiliation: Children's Hospital Boston, Renal Division, Harvard Medical School, Boston, Massachusetts, United States of America.
authors.forename: Brian
authors.initials: B
authors.lastname: Smith
authors.affiliation: Department of Immunology, Juntendo University, Tokyo, Japan.
authors.forename: Hisaya
authors.initials: H
authors.lastname: Akiba
authors.affiliation: Department of Immunology, Juntendo University, Tokyo, Japan.
authors.forename: Hideo
authors.initials: H
authors.lastname: Yagita
authors.affiliation: Children's Hospital Boston, Renal Division, Harvard Medical School, Boston, Massachusetts, United States of America.
authors.forename: Indira
authors.initials: I
authors.lastname: Guleria
mesh_terms: D000818:Animals; D000950:Antigens, Ly / Q000378:metabolism; D039481:CD11b Antigen / Q000378:metabolism; D002478:Cells, Cultured; D018925:Chemokines / Q000378:metabolism; D005260:Female; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000502:physiology; D000072597:Hepatitis A Virus Cellular Receptor 2; D054502:Histocompatibility, Maternal-Fetal; D007108:Immune Tolerance; D016130:Immunophenotyping; D019409:Interleukin-15 / Q000378:metabolism; D007694:Killer Cells, Natural; D008297:Male; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA; D010920:Placenta / Q000276:immunology / Q000378:metabolism; D011247:Pregnancy; D011991:Receptors, Virus / Q000502:physiology*; D014599:Uterus / Q000166:cytology* / Q000276:immunology / Q000378:metabolism
chemical_list: D000950:Antigens, Ly; D039481:CD11b Antigen; D018925:Chemokines; C442241:Havcr2 protein, mouse; D000072597:Hepatitis A Virus Cellular Receptor 2; D019409:Interleukin-15; C526827:Ly6 protein, mouse; D011991:Receptors, Virus; D016178:Granulocyte-Macrophage Colony-Stimulating Factor