Treatment of Brucella-susceptible mice with IL-12 increases primary and secondary immunity

Crucial Role of Gamma Interferon-Producing CD4+Th1 Cells but Dispensable Function of CD8+T Cell, B Cell, Th2, and Th17 Responses in the Control of Brucella melitensis Infection in Mice

“…Thus, we conclude that the low levels of IL-4 produced during Brucella infection in wild-type C57BL/6 and BALB/c mice do not affect the ability to mount a protective response. These observations support the idea, previously suggested by others (62), that the susceptibility of BALB/c mice to Brucella infection is not due to the development of a Th2 response but is due to an intrinsically lower ability to mount a Th1 response.…”

Interleukin-1 Receptor-Associated Kinase 4 Is Essential for Initial Host Control of Brucella abortus Infection

“…The recognition of pathogens by TLRs leads to an immune response that culminates in the production of the proinflammatory cytokines, amplification of the innate immune response, and activation of the adaptive immune system (2). Furthermore, IL-12 and IFN-␥ are directly related to control of infection with B. abortus (24,32,41). In this context, a better understanding of how TLR signaling events are initiated and how they are transduced within the cell provides important information to help decipher the puzzle of host-Brucella relationship.…”

“…The immune response against Brucella infection involves many molecules and cells to trigger a Th1 immune response and activation of CD8 ϩ T cells (12,26,27). Furthermore, gamma interferon (IFN-␥) is essential for host control of Brucella infection (24,32,41).…”

The quest for a true One Health perspective of brucellosis

“…results in a decrease in the IFN-γ response after the first week of infection (33). The production of IFN-γ can be partially rescued by administering recombinant interleukin-12 (IL-12) (33), which is made by cells of the innate immune system, and activation of those cells via tolllike receptors (TLRs), particularly TLR2 and TLR4 (34).…”