Brucella abortus induces apoptosis of human T lymphocytes.

VELÁSQUEZ L.N.; DELPINO, M.V.; IBAÑEZ A.; CORIA M.L.; MIRAGLIA M. C.; SCIAN R.; CASSATARO J.; GIAMBARTOLOMEI G.H.; BARRIONUEVO P.

MICROBES AND INFECTION

ELSEVIER SCIENCE BV

Lugar: Amsterdam; Año: 2012 vol. 14 p. 639 - 650

1286-4579

Immune evasion is essential for Brucella abortus to survive in the face of robust adaptive CD4þ T cell response. We have previously demonstrated that B. abortus can indirectly inhibit CD4þ T cells by down-regulating MHC-II expression and antigen presentation on macrophages. However, whether B. abortus is able to directly interfere with T lymphocytes is not known. We report here that B. abortus induces apoptosis of human T lymphocytes, even though invasion of T lymphocytes was low and non-replicative. The ability of heat-killed B. abortus to reproduce the same phenomenon suggested that there was a bacterial structural component involved. We demonstrated that a prototypical B. abortus outer membrane lipoprotein (L-Omp19), but not its unlipidated form, induced T lymphocyte apoptosis. Moreover, a synthetic lipohexapeptide that mimics the structure of the protein lipid moiety also induced an increase in T lymphocyte cell death, indicating that the structural component implicated in the phenomenon could be any B. abortus lipoprotein. B. abortus-induced T lymphocyte apoptosis was dependent on the secretion of TNF-a since pre-incubation of T lymphocytes with anti-TNF-a mAb inhibited the apoptosis of the cells. Overall,these results represent a new mechanism whereby B. abortus by directly inhibiting T cell-mediated responses may evade adaptive immuneresponses