IDEHU   05542
INSTITUTO DE ESTUDIOS DE LA INMUNIDAD HUMORAL PROF. RICARDO A. MARGNI
Unidad Ejecutora - UE
artículos
Título:
Brucella lipoproteins mimic dendritic cell maturation induced by Brucella abortus
Autor/es:
ZWERDLING A,; DELPINO MV; BARRIONUEVO P,; CASSATARO J; PASQUEVICH K; SAMARTINO C, GARCIA; FOSSATI CA; GIAMBARTOLOMEI GH
Revista:
MICROBES AND INFECTION
Referencias:
Año: 2008 vol. 12 p. 1559 - 1565
ISSN:
1286-4579
Resumen:
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The strategies that allow Brucella abortus to
survive inside macrophages for prolonged periods and to avoid the
immunological surveillance of major histocompatibility complex class II
(MHC-II)-restricted gamma interferon (IFN-_)-producing
CD4_ T lymphocytes are poorly
understood. We report here that infection of THP-1 cells with B. abortus
inhibited expression of MHC-II molecules and antigen (Ag) processing. Heat-killed B.
abortus (HKBA) also induced both these phenomena, indicating the
independence of bacterial viability and involvement of a structural
component of the bacterium. Accordingly, outer membrane protein 19 (Omp19), a prototypical
B. abortus lipoprotein, inhibited both MHC-II expression and Ag
processing to the same extent as HKBA. Moreover, a synthetic
lipohexapeptide that mimics the structure of the protein lipid moiety also inhibited
MHC-II expression, indicating that any Brucella lipoprotein could
down-modulate MHC-II expression and Ag processing. Inhibition of MHC-II
expression and Ag processing by either HKBA or lipidated Omp19 (L-Omp19)
depended on Toll-like receptor 2 and was mediated by interleukin-6. HKBA or
L-Omp19 also inhibited MHC-II expression and Ag processing of human
monocytes. In addition, exposure to the synthetic lipohexapeptide
inhibited Ag-specific T-cell proliferation and IFN-_ production
of peripheral blood mononuclear cells from Brucella-infected
patients. Together, these results indicate that there is a mechanism by
which B. abortus may prevent recognition by T cells to evade host
immunity and establish a chronic infection.