Brucella abortus induces apoptosis of human T lymphocytes

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• 作者：Lis N. Velá ; squez^a ; ^b ; M. Victoria Delpino^a ; ^b ; André ; s E. Ibañ ; ez^a ; ^b ; Lorena M. Coria^a ; ^b ; M. Cruz Miraglia^a ; ^b ; Romina Scian^a ; ^b ; Juliana Cassataro^a ; ^b ; Guillermo H. Giambartolomei^a ; ^b ; Paula Barrionuevo^a ; ^b ; ^{pbarrion2004@yahoo.com.ar}
• 关键词：Brucella abortus ; Lipoproteins ; Apoptosis ; T lymphocytes
• 刊名：Microbes and Infection
• 出版年：2012
• 期刊代码：65_12864579
• 类别：imm
• 出版时间：July, 2012
• 卷：14
• 期：7-8
• 页码：639-650
• 文件大小：1372 K

摘要

Immune evasion is essential for m>Brucella abortusm> to survive in the face of robust adaptive CD4+ T cell response. We have previously demonstrated that m>B. abortusm> can indirectly inhibit CD4+ T cells by down-regulating MHC-II expression and antigen presentation on macrophages. However, whether m>B. abortusm> is able to directly interfere with T lymphocytes is not known. We report here that m>B. abortusm> induces apoptosis of human T lymphocytes, even though invasion of T lymphocytes was low and non-replicative. The ability of heat-killed m>B. abortusm> to reproduce the same phenomenon suggested that there was a bacterial structural component involved. We demonstrated that a prototypical m>B.聽abortusm> 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 m>B. abortusm> lipoprotein. m>B. abortusm>-induced T lymphocyte apoptosis was dependent on the secretion of TNF-伪 since pre-incubation of T lymphocytes with anti-TNF-伪 mAb inhibited the apoptosis of the cells. Overall, these results represent a new mechanism whereby m>B. abortusm> by directly inhibiting T cell-mediated responses may evade adaptive immune responses.