| Autor: |
Stevens, Anne M., Howsmon, Rebecca, Gadi, Vijayakrishna K., Gammill, Hilary S., Lambert, Nathalie C., Sunku, Chennakesava C., Hermes, Heidi M. Hermes, Porter, Allison J., Lu, Christine, Nelson, J.Le |
| Předmět: |
|
| Zdroj: |
Chimerism; Apr-Jun2013, Vol. 4 Issue 2, p51-51, 1p |
| Abstrakt: |
Background. Persistent circulating microchimerism with allogeneic cells can be derived from transplanted solid organs, blood transfusions, or maternal-fetal exchange. Male microchimerism has been detected in women with SLE who have given birth to sons, but also in nulligravid women with putative sources including unrecognized pregnancy or a vanished twin. We hypothesized that male microchimerism in pre-pubescent girls may be attributed to older siblings. Methods. Peripheral blood mononuclear cells from 81 pediatric SLE patients and 34 age-matched controls were assayed for microchimerism by Real-Time QPCR amplification of the Y-chromosome derived DYS14 and HLA and GST sequences. As autoimmune comparison groups, 40 children with scleroderma and 29 with juvenile idiopathic arthritis (JIA) were studied. Male cells were detected in tissue by fluorescence in situ hybridization for Y-chromosome sequences. Disease activity was measured by the SLE Disease Activity Index. Results. Male microchimerism was detected with increased frequency in SLE, (34% of SLE patients compared with 11.8% of healthy controls p = 0.02). The mean levels of DNA were not significantly higher (32 genome equivalents per million (gEq/M) in SLE vs. 15.5 gEq/M in controls, p = 0.14). In pre-pubertal girls who could never have been pregnant, the level of male microchimerism tended to be higher in SLE, but the difference was not significant. Male DNA was detected in 40% of pre-pubertal SLE patients compared with 14.3% of controls (p = 0.15), with a mean of 35.4 gEq/M in SLE vs. 13.1 gEq/M in controls, (p = 0.2). Male cells were detected in one of seven female kidney biopsy samples assayed, derived from a 5 y-old girl with newly- diagnosed SLE. Male DNA was not elevated in children with scleroderma or JIA compared with controls. No association was found between microchimerism levels and disease activity, race, prematurity, or prior transfusion. In four of six patients with male microchimerism a non-shared GST or HLA sequence carried by an older brother was also detected. Conclusion. Girls with SLE harbor male microchimerism in the blood, and in one affected kidney. In some cases the source may be indirectly from an older brother through the mother. Loss of tolerance to non-shared male antigens could lead to chronic activation of host T lymphocytes, with subsequent autoimmunity through a mechanism of epitope spreading, similar to the graft-vs.-host disease seen after stem cell transplantation. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
|
