Saturday, October 28, 2006
Protecting Mothers From Fetal Immune Recognition
Nashville (USA), 26 October: A protein expressed in developing embryos may protect mothers against immune-mediated attack by fetal cells, according to a study to be published in December issue of Nature Immunology. This protein, called Zfp608, appears to function by switching off the ex-pression of Rag genes, which are involved in the development and function of fetal immune cells.
Thomas Aune and colleagues identified Zfp608 by honing in on a genetic defect exhibited by a strain of mice called ZORI, which have a compromised immune system. These mice have reduced numbers of T lymphocytes, immune cells that develop in the thymus. Normally mice express Zfp608 during embryonic development but stop its ex-pression soon after birth. In contrast, ZORI mice continue to express Zfp608 in their thymus well beyond birth; continued Zfp608 ex-pression is therefore linked to lack of thymic immune cell development.
The authors show that Zfp608 inhibits Rag gene ex-pression in thymic cells, which explains the defect in T lymphocyte development observed in ZORI mice. They speculate that the timing of Zfp608 ex-pression in embryos might play a protective role by preventing the development of fetal immune cells that could potentially recognize and attack maternal tissues, thereby harming both mother and her unborn offspring.
The authors show that Zfp608 inhibits Rag gene ex-pression in thymic cells, which explains the defect in T lymphocyte development observed in ZORI mice. They speculate that the timing of Zfp608 ex-pression in embryos might play a protective role by preventing the development of fetal immune cells that could potentially recognize and attack maternal tissues, thereby harming both mother and her unborn offspring.
(ResearchSEA)
Thomas Aune and colleagues identified Zfp608 by honing in on a genetic defect exhibited by a strain of mice called ZORI, which have a compromised immune system. These mice have reduced numbers of T lymphocytes, immune cells that develop in the thymus. Normally mice express Zfp608 during embryonic development but stop its ex-pression soon after birth. In contrast, ZORI mice continue to express Zfp608 in their thymus well beyond birth; continued Zfp608 ex-pression is therefore linked to lack of thymic immune cell development.
The authors show that Zfp608 inhibits Rag gene ex-pression in thymic cells, which explains the defect in T lymphocyte development observed in ZORI mice. They speculate that the timing of Zfp608 ex-pression in embryos might play a protective role by preventing the development of fetal immune cells that could potentially recognize and attack maternal tissues, thereby harming both mother and her unborn offspring.
The authors show that Zfp608 inhibits Rag gene ex-pression in thymic cells, which explains the defect in T lymphocyte development observed in ZORI mice. They speculate that the timing of Zfp608 ex-pression in embryos might play a protective role by preventing the development of fetal immune cells that could potentially recognize and attack maternal tissues, thereby harming both mother and her unborn offspring.
(ResearchSEA)
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