This chapter describes the immunological response to Brucella. The host immune response to Brucella is divided into innate and adaptive immunity. Protection against Brucella infection requires cell-mediated immunity, which includes CD4+ and CD8+ T lymphocytes, Th1-type cytokines such as IFN-γ and tumor necrosis factor-alpha (TNF-α), and activated macrophages and dendritic cells. Neutrophils, CD8+ and γδ T cells are part of the secondary innate immune response and migrate in the early stages of the infection to contribute to resolve the infection. Cytokine expression is necessary for development of a protective immune response. Brucella induces minimal production of pro-inflammatory cytokines. TNF-α, IL-12, and IFN-γ are the primary cytokines critical for defense against Brucella. In brucellosis, immune response mechanisms are divided in three primary mechanisms: (1) in the first step, it inhibits the intracellular survival of Brucella, IFN-γ produced by CD4+, CD8+, and T cells which activate macrophages, enhancing their bactericidal capacity; (2) secondly, cytotoxic CD8+ T cells directly kill infected macrophages, and T cells; and (3) thirdly, B lymphocytes secrete antibodies, in the endocytic compartments opsonization of Brucella and occur by immunoglobulin (Ig) G2a and IgG3 to increase phagocytosis which is useful for diagnosis of disease. The humoral antibody response consists in an early production of IgM against Brucella LPS for 3 to 4 weeks and rises gradually during the course of acute infection, followed by a gradual increase in IgG and IgA, beginning 7 to 14 days after infection. The dominant IgG isotype is IgG2. Antibodies against Brucella are proteins that cause agglutination, complement fixation, and precipitation when reacted with their homologous antigens. These antibodies have the potential to produce cross-reactions and this inevitably results in false positive serological tests.
