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ShareApr. 22, 2010 — Fetuses and infants are highly susceptible to viral infections. A number of viruses, including human cytomegalovirus (CMV), cause more severe disease in early life compared to later life.
CMV is the most common cause of infection of the fetus: about 1 in 100 newborns are infected. Although CMV infection causes no detectable symptoms in immunocompetent adults, about 20% of CMV-infected newborns develop serious symptoms, including cerebral malformations, multiple organ failure, deafness, and mental retardation. It is generally accepted that this increased susceptibility to viral infections is related to the immaturity of the neonatal immune system.
T cells are a part of the cellular immune system that is important to fight viral infections. γδ T cells are unconventional T cells: they do not recognize pieces of pathogen proteins (for example from viruses) as conventional ab T cells do. In fact, it is largely unknown what γδ T cell receptors recognize.
At the Institute for Medical Immunology (Université Libre de Bruxelles), in collaboration with clinicians from Hôpital Erasme and Le Centre Hospitalier Universitaire Saint-Pierre, they have found that human fetal γδ T cells can mount a vigorous response to CMV infection during development in utero. They discovered a novel anti-CMV γδ T cell receptor that was highly expanded in CMV-infected fetuses. Thus γδ T cells can provide an important mechanism by which the fetus fights pathogens and they could be a target for the design of novel vaccination strategies against infection in early life.
This study has been published in The Journal of Experimental Medicine.
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The above story is reprinted from materials provided by Libre de Bruxelles, Universit, via AlphaGalileo.
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Journal Reference:
- D. Vermijlen, M. Brouwer, C. Donner, C. Liesnard, M. Tackoen, M. Van Rysselberge, N. Twite, M. Goldman, A. Marchant, F. Willems. Human cytomegalovirus elicits fetal γδ T cell responses in utero. Journal of Experimental Medicine, 2010; 207 (4): 807 DOI: 10.1084/jem.20090348
Note: If no author is given, the source is cited instead.
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