Washington, Apr 25 (ANI): Recent studies at University of Washington (UW) have suggested that specialized types of white blood cells, a category called regulatory T cells might put a halt to the body's autoimmune response, a cellular self-attack, by directing first responders to the site of viral infection.

T-cells are important in controlling autoimmunity, a cellular self-attack that can lead to diseases like reactive arthritis.

UW researchers have shown in a rodent study that young mice deficient in regulatory T cells die from an aggressive form of autoimmunity that damages several organs.

Alexander Y. Rudensky, professor of immunology at UW has said that while there's a great interest in the therapeutic potential of regulatory T cells, studies in lab animals suggest these cells might be harnessed to treat autoimmune diseases or reduce rejection of transplanted organs.

According to the researchers, regulatory T cells might call a halt to immune responses as the body nears success in eliminating an infection. This suppression as the fight draws to an end would reduce tissue damage from robust immune responses.

In the recent study, namely "Coordination of Early Protective Immunity to Viral Infections by Regulatory T Cells," researchers scouted for a role for regulatory T cells during the start of a herpes simplex virus infection in mucus membranes.

When regulatory T cells are deficient in mice, the herpes simplex virus replicates rapidly in the mucus membranes and spreads to the spinal cord. On a closer examination of these mice that lack regulatory T cells, the researchers found very little interferon, an anti-viral chemical that also boosts the immune response, at the infection site, even though it was found in the draining lymph nodes.

They also noticed that in the lymph nodes there was a sharp increase in certain chemokines, chemicals that stimulate immune cells to move in and cause inflammation. Besides, a delay was also noticed in killer cells, dendritic cells (the cells that capture and present foreign proteins to other immune cells), and T cells arriving at the site of infection, where they were supposed to go earlier to fulfill their virus-fighting roles.

Thus it was suggested that a possible reason for this tardiness is an alteration in the chemical cues necessary for these cells to migrate to the site of infection. The authors described the finding of an immune-response promoting role for regulatory T cells during the early stages of a local infection as "unexpected," considering the cells' suppressor roles during later stages of an immune response.

Their findings appear in the latest edition of Science Express, a Web edition of selected Science papers published in advance of the print edition. (ANI)