scispace - formally typeset
A

André Báfica

Researcher at Universidade Federal de Santa Catarina

Publications -  78
Citations -  4816

André Báfica is an academic researcher from Universidade Federal de Santa Catarina. The author has contributed to research in topics: Mycobacterium tuberculosis & Immune system. The author has an hindex of 34, co-authored 72 publications receiving 4456 citations. Previous affiliations of André Báfica include Oswaldo Cruz Foundation & National Institutes of Health.

Papers
More filters
Journal ArticleDOI

TLR9 regulates Th1 responses and cooperates with TLR2 in mediating optimal resistance to Mycobacterium tuberculosis

TL;DR: A previously unappreciated role for TLR9 is revealed in the host response to M. tuberculosis and TLR collaboration in host resistance to a major human pathogen is illustrated.
Journal ArticleDOI

Anti-inflammatory actions of lipoxin A4 and aspirin-triggered lipoxin are SOCS-2 dependent.

TL;DR: It is shown that lipoxins activate two receptors in DCs, AhR and LXAR, and that this activation triggers expression of suppressor of cytokine signaling (SOCS)-2, which is a crucial intracellular mediator of the anti-inflammatory actions of aspirin-inducedlipoxins in vivo.
Journal ArticleDOI

Cutting edge: TLR9 and TLR2 signaling together account for MyD88-dependent control of parasitemia in Trypanosoma cruzi infection.

TL;DR: The results reveal that TLR2 and TLR9 cooperate in the control of parasite replication and thatTLR9 has a primary role in the MyD88-dependent induction of IL-12/IFN-γ synthesis during infection with T. cruzi.
Journal ArticleDOI

Intranasal Poly-IC treatment exacerbates tuberculosis in mice through the pulmonary recruitment of a pathogen-permissive monocyte/macrophage population

TL;DR: The above findings suggest that Poly-ICLC treatment can detrimentally affect the outcome of M. tuberculosis infection, by promoting the accumulation of a permissive myeloid population in the lung.
Journal ArticleDOI

Host control of Mycobacterium tuberculosis is regulated by 5-lipoxygenase-dependent lipoxin production.

TL;DR: It is demonstrated that lipoxins negatively regulate protective Th1 responses against mycobacterial infection in vivo and suggested that the inhibition of lipoxin biosynthesis could serve as a strategy for enhancing host resistance to M. tuberculosis.