V gamma 9V delta 2 T cells in human legionellosis

In humans, expansion of circulating V gamma 9V delta2 T cells seems to be a pathophysiological denominator shared by protozoan and intracellular bacte rial diseases. The assumption was tested here on legionellosis, a condition conforming to the category but not yet described with respect to gamma del ta T cells. Levels of V gamma 9V delta2 T cells in peripheral blood were me asured at various intervals in 14 subjects undergoing a Pontiac fever-like disease, shown by serological investigation to be caused by Legionella micd adei. In samples obtained 4 to 6 days after the onset of the disease, the m ean percentage ( the standard deviation) of V gamma 9V delta2(+) T cells am ong CD3(+) cells was 1.0% +/- 0.5%, compared to 5.0% +/- 3.9% in healthy co ntrol subjects (P < 0.001). Thereafter, a pronounced increase occurred and at 2 to 7 weeks after onset, mean peak levels were as high as <approximate to> 15%. During the next 6 months, values slowly declined, although without reaching the normal range. Percentages of gamma delta (+) T cells expressi ng tumor necrosis factor alpha or gamma interferon in response to phorbol m yristate acetate were assayed in vitro. At 14 to 16 days after the onset of disease, the expression of both cytokines was increased (P < 0.01), wherea s at 5 to 7 weeks, the expression of tumor necrosis factor alpha was decrea sed (P < 0.05), possibly reflecting modulation of an inflammatory response. In conclusion, Pontiac fever was found to be associated with a pronounced and long-lasting expansion of V gamma 9V delta2 T cells, implying that the subset may also be pathophysiologically important in a mild and transient f orm of intracellular bacterial diseases. Surprisingly, the expansion was pr eceded by a depletion of circulatory V gamma 9V delta2 T cells. Possibly, V gamma 9V delta2 T cells are initially recruited to a site of infection bef ore they expand in response to antigen and occur in high numbers in blood.