title: Fetal cell microchimerism in tissue from multiple sites in women with systemic sclerosis.
abstract: OBJECTIVE
  The realization that fetal cells pass into the maternal circulation and can survive for many years has raised the question of whether fetal microchimerism can cause subsequent disease in the mother. Available data suggest that fetal-maternal transfusion may be related to some autoimmune diseases, notably systemic sclerosis (SSc). The goal of the current work was to identify and quantify tissue-specific fetal microchimerism in women with SSc.
  
  
  METHODS
  We analyzed multiple tissue specimens obtained at autopsy from women with SSc as well as women who had died of causes unrelated to autoimmunity, using fluorescence in situ hybridization to detect the presence of male cells in women with sons. Tissues analyzed included adrenal gland, heart, intestine, kidney, liver, lung, lymph node, pancreas, parathyroid, skin, and spleen.
  
  
  RESULTS
  Male cells were observed in tissue from at least 1 site in each woman with SSc and were found most frequently in spleen sections. After spleen, male cells were observed most frequently in lymph node, lung, adrenal gland, and skin tissue. The only tissue type in which male cells were not seen in any patient was pancreatic tissue. Male cells were not observed in tissue from women who had died of causes unrelated to autoimmunity.
  
  
  CONCLUSIONS
  The results of this study suggest that fetal cells migrate from the peripheral circulation into multiple organs in women with SSc. All of the women studied had previously given birth to sons, so it is likely that these cells are of fetal origin. While the relevance of this finding to the pathogenesis of SSc remains to be elucidated, the presence of fetal cells in internal organs suggests that they could play a role in disease pathogenesis and that they may preferentially sequester in the spleen. The presence of these male cells may also be a result of disease, possibly through the migration of terminally differentiated and/or progenitor cells to areas of tissue damage.
authors.affiliation: New England Medical Center and Tufts University, Boston, Massachusetts 02111, USA.
authors.forename: K L
authors.initials: KL
authors.lastname: Johnson
authors.forename: J L
authors.initials: JL
authors.lastname: Nelson
authors.forename: D E
authors.initials: DE
authors.lastname: Furst
authors.forename: P A
authors.initials: PA
authors.lastname: McSweeney
authors.forename: D J
authors.initials: DJ
authors.lastname: Roberts
authors.forename: D K
authors.initials: DK
authors.lastname: Zhen
authors.forename: D W
authors.initials: DW
authors.lastname: Bianchi
mesh_terms: D000328:Adult; D000368:Aged; D002467:Cell Nucleus / Q000737:chemistry; D002678:Chimera / Q000235:genetics; D005260:Female; D005333:Fetus / Q000166:cytology*; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D008297:Male; D008431:Maternal-Fetal Exchange; D008875:Middle Aged; D011247:Pregnancy; D012595:Scleroderma, Systemic / Q000209:etiology* / Q000235:genetics; D013154:Spleen / Q000737:chemistry; D014018:Tissue Distribution; D014998:Y Chromosome