[4] A 2012 study at the Fred Hutchinson Cancer Research Center, Seattle, has detected cells with the Y chromosome in multiple areas of the brains of deceased women.
[11] Microchimerism had also been shown to exist after blood transfusions to a severely immunocompromised population of patients who suffered trauma.
Microchimerism provides a method of diagnosing the condition, because male genetic material can be detected in a blood sample.
For example, condition of women suffering from autoimmune disorders (e.g. rheumatoid arthritis, multiple sclerosis) improves during pregnancy.
[18][19] These changes in immune responses during pregnancy extend to maternal components specific to fetal antigens, because of feto-maternal cell transfer and their retention in mother tissues.
[26] This expanded immune tolerance persists in both mother and offspring after birth and allows microchimeric cells to be retained in tissues.
NIMA-specific tolerance causes some interesting immunological phenotypes: sensitization to erythrocyte Rhesus factor (Rh) antigens is reduced among Rh- women born to Rh+ women,[27] long-term kidney allograft survival is improved in NIMA-matched donor-recipient sibling pairs,[28] or acuteness of bone marrow transplantation graft-versus-host disease is reduced, when recipients of donor stem cells are NIMA-matched.
[29] Cross-fostering animal studies show that when postnatal NIMA exposure though breastfeeding is eliminated, survival of NIMA-matched allografts is reduced.
[30] The severity of preexisting autoimmune disorders is reduced during pregnancy and it is most apparent when fetal microchimeric cells levels are highest - during the last trimester.
Independent studies repeatedly suggested that microchimeric cells of fetal origin may be involved in the pathogenesis of systemic sclerosis.
[35] Contrarily, an alternative hypothesis on the role of microchimeric cells in lesions is that they may be facilitating tissue repair of the damaged organ.
[36] Moreover, fetal immune cells have also been frequently found in breast cancer stroma as compared to samples taken from healthy women.
Women with lupus nephritis containing male fetal cells in their kidney biopsies exhibited better renal system functioning.
[39] In contrast, women without male fetal cells who had lupus nephritis showed a more serious form of glomerulonephritis and higher levels of serum creatinine.
[39] The specific role that fetal cells play in microchimerism related to certain autoimmune diseases is not fully understood.
Studies showed the presence of Y-chromosome-positive fetal cells in minor salivary glands in 11 of 20 women with SS but in only one of eight normal controls.
LP is characterized by T lymphocytes infiltration of the lower levels of epithelium, where they damage basal cells and cause apoptosis.
The fetal microchimerism may trigger a fetus versus host reaction and therefore may play a role in the pathogenesis of autoimmune diseases including LP.
Study of S. Hallum shows association between male origin fetal cells and ovarian cancer risk.
Microchimerism is a result of pregnancy, possibility that foreign cells were of transfusion or transplantation origin was rejected due to women's health.
Microchimeric cells might induce the alteration of the woman's immune system and make the cervical tissue more susceptible to HPV infection or provide a suitable environment for tumor growth.
[54] Microchimeric fetal cells expressed collagen I, III and TGF-β3, and they were identified in healed maternal cesarean section scars.
This suggests that these cells migrate to the site of damage due to maternal skin injury signals, and help repair tissue.
[55] Fetomaternal microchimerism has been shown in experimental investigations of whether fetal cells can cross the blood brain barrier in mice.
Hormonal changes in pregnancy alter neurogenesis, which could create favorable environments for fetal cells to respond to injury.