Gene Linked to Age-Related Loss of Immune Function Identified

A recent paper described the identification of a gene and its protein that stimulate the transformation of undifferentiated white blood cell progenitors into mature T-cells, a finding that may help to reverse the age-related decline in the efficacy of the immune response.

The loss of immune cell function is partially due to thymic atrophy, which is typified by decreased output of T-cells from the thymus and by the decreased ability to recognize new antigens.
Investigators at the University of Montreal (QB, Canada) studied the role of the Wnt4 gene and its protein product in thymopoiesis, the pathway leading to production of T-cells in the thymus. They reported in the July 2008 issue of the journal Immunity that gain-of-function and loss-of-function models showed that Wnt4 differentially affected diverse subsets of hematopoietic stem and progenitor cells. Elevated levels of Wnt4 led to a marked increase in the number of white blood cell progenitors and of immature T-cells in the thymus in particular. Contrarily, deletion of the Wnt4 gene and lack of the corresponding protein was associated with a decrease in the number of T-cell progenitors in the thymus.
"Thymic atrophy is a major public health problem,” said senior author Dr. Claude Perreault, professor of immunology at the University of Montreal. "It compromises the efficacy of vaccination and weakens the resistance to common viruses, for instance to the respiratory syncytial virus (RSV), which is responsible each year for the hospitalization of more than 150,000 people in the U.S. This is due to the fact that old T-cells are not equipped to face the threat of new foreign bodies, whether they are viruses or tumors.”


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