Hindawi Publishing Corporation Clinical and Developmental Immunology Volume 2012, Article ID 589494, 7 pages doi:10.1155/2012/589494 Research Article Host Susceptibility to Brucella abortus Infection Is More Pronounced in IFN-γ knockout than IL-12/β2-Microglobulin Double-Deficient Mice Ana Paula M. S. Brand˜ ao, 1 Fernanda S. Oliveira, 1 Natalia B. Carvalho, 1 Leda Q. Vieira, 1 Vasco Azevedo, 2 Gilson C. Macedo, 3 and Sergio C. Oliveira 1 1 Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, 31270-901 Belo Horizonte, MG, Brazil 2 Department of General Biology, Institute of Biological Sciences, Federal University of Minas Gerais, 31270-901 Belo Horizonte, MG, Brazil 3 Department of Parasitology, Microbiology and Immunology, Biological Sciences Institute, Federal University of Juiz de Fora, 36036-900 Juiz de Fora, MG, Brazil Correspondence should be addressed to Sergio C. Oliveira, scozeus@icb.ufmg.br Received 28 July 2011; Accepted 19 September 2011 Academic Editor: Georgios Pappas Copyright © 2012 Ana Paula M. S. Brand˜ ao et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Brucella abortus is a facultative intracellular bacterial pathogen that causes abortion in domestic animals and undulant fever in humans. IFN-γ, IL-12, and CD8+ T lymphocytes are important components of host immune responses against B. abortus. Herein, IFN-γ and IL-12/β2-microglobulin (β2-m) knockout mice were used to determine whether CD8+ T cells and IL-12-dependent IFN-γ deficiency would be more critical to control B. abortus infection compared to the lack of endogenous IFN-γ. At 1 week after infection, IFN-γ KO and IL-12/β2-m KO mice showed increased numbers of bacterial load in spleens; however, at 3 weeks postinfection (p.i.), only IFN-γ KO succumbed to Brucella. All IFN-γ KO had died at 16 days p.i. whereas death within the IL- 12/β2-m KO group was delayed and occurred at 32 days until 47 days postinfection. Susceptibility of IL-12/β2-m KO animals to Brucella was associated to undetectable levels of IFN-γ in mouse splenocytes and inability of these cells to lyse Brucella-infected macrophages. However, the lack of endogenous IFN-γ was found to be more important to control brucellosis than CD8+ T cells and IL-12-dependent IFN-γ deficiencies. 1. Introduction Brucella is a Gram-negative bacterium which is pathogenic to humans and animals [1]. The establishment on infection depends of entrance of this bacterium through the nasal, oral, and/or conjunctival mucosa. After entering into the host cells, Brucella has the ability to infect and multiply in phagocytic and nonphagocytic cells [2, 3]. However, macrophages are considered the main cells of Brucella residence in the host [4]. The immune response against Brucella infection involves many molecules and cells to trigger a Th1 immune response and activation of CD8+ T cells [5–7]. IFN-γ is a critical cytokine for host control of Brucella infection [8–10]. The importance of IFN-γ to control Bru- cella was first shown in vivo with monoclonal antibodies that depleted or neutralized IFN-γ in mice [10–12]. Subsequently, a more dramatic role was shown by using IFN-γ KO mice when both BALB/c and C57BL/6 mice died after infection with B. abortus strain S2308 [8]. CD4+ T cells are the major producers of IFN-γ in brucellosis, although other subsets such as CD8+ T cells also contribute [7, 13]. A number of studies have demonstrated a role for either CD4+ or CD8+ T cells in the control of brucellosis [7, 14]. In adoptive transfer studies, CD8+ and CD4+ T cells have been shown to be equally protective for resistance to infection with virulent