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- Infection with Brucella abortus has been shown to potently activate both the innate and adaptive arms of the immune system, leading to a proinflammatory response that favors the differentiation of T-cell responses toward a T-helper 1 (Th1) profile (15,(55)(56)(57). Despite this immune response, B. abortus can persist for years inside macrophages, evading host immune responses.IIMacrophages are an early barrier for defense against Brucella. They phagocytose and degrade invading microorganisms, participating actively in innate immunity. Additionally, by processing microorganisms within intracellular compartments, they present peptides in the context of the major histocompatibility complex (MHC) to T lymphocytes, promoting the adaptive immune response. Gamma interferon (IFN-␥) has a critical role in protective immunity against Brucella. This cytokine enhances both the microbicidal and antigen-presenting functions of macrophages (12,18,19,48). Thus, the virulence of B. abortus relies on the ability of this organism to survive and replicate within vacuolar phagocytic compartments of macrophages (26,30), and the macrophage-Brucella interaction is critical for the establishment of chronic Brucella infections.
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