Brucella spp., are Gram negative bacteria that cause disease by growing within monocyte/macrophage lineage cells. Clinical manifestations of
brucellosis are immune mediated, not due to bacterial
virulence factors. Acquired immunity to
brucellosis has been studied through observations of naturally infected hosts (cattle, goats), mouse models (mice), and human
infection. Even though Brucella spp. are known for producing mechanisms that evade the immune system, cell-mediated immune responses drive the clinical manifestations of human disease after exposure to Brucella species, as high antibody responses are not associated with protective immunity. The precise mechanisms by which cell-mediated immune responses confer protection or lead to disease manifestations remain undefined. Descriptive studies of immune responses in human
brucellosis show that TH(1) (
interferon-γ-producing T cells) are associated with dominant immune responses, findings consistent with animal studies. Whether these T cell responses are protective, or determine the different clinical responses associated with
brucellosis is unknown, especially with regard to
undulant fever manifestations, relapsing disease, or are associated with responses to distinct sets of Brucella spp.
antigens are unknown. Few data regarding T cell responses in terms of specific recognition of Brucella spp.
protein antigens and peptidic
epitopes, either by CD4+ or CD8+ T cells, have been identified in human
brucellosis patients. Additionally because current attenuated Brucella
vaccines used in animals cause human disease, there is a true need for a
recombinant protein subunit vaccine for human
brucellosis, as well as for improved diagnostics in terms of prognosis and identification of unusual forms of
brucellosis. This review will focus on current understandings of
antigen-specific immune responses induced Brucella peptidic
epitopes that has promise for yielding new insights into
vaccine and diagnostics development, and for understanding pathogenetic mechanisms of human
brucellosis.