Dandekar had been studying the role of gut-associated lymphoid tissue in HIV. In a 2006 study, she found that HIV continued to replicate in the gut mucosa and suppress immune function in patients being treated with antiretroviral therapy even when T-cell counts from blood samples from the same individuals indicated antiretroviral treatment was working.
We think the real battle between an individuals immune system and HIV is happening in the gut mucosa where there is massive destruction of immune cells, Dandekar said. Gut-associated lymphoid tissue, she pointed out, accounts for 70 percent of the bodys immune system.
In HIV-infected patients, there is a gradual loss of CD4+ T cells over time. These cells, also called T helper cells, organize the immune systems attack on disease-causing invaders, like Salmonella. Unlike the steady decline of T cells in peripheral blood, there is a very rapid loss of CD4+ T cells in the gut mucosa, Dandekar said.
We wanted to know whether the loss of the CD4+ T-cells in the gut contributed to the inactivation of the immune system one sees in HIV-infected patients, she said.
Both Bumler and Dandekar said the timing was perfect for their collaboration. Together, they developed a novel technique that allowed them to study early intestinal responses to Salmonella infection in rhesus macaques infected with simian immunodeficiency virus (SIV), an established model for HIV infection.
We found that animals that had no SIV infection were able to generate immediate responses to bacterial exposure, producing Th17 cells in large amounts, Dandekar said. The SIV-infected animals, however, had either a significantly lower response or lacked did not produce measurable amounts of th
|Contact: David Ong|
University of California - Davis - Health System