Here, we discuss the modulation of inflammation upon pathogen invasion, including the new pathway triggered by lipoxin involved in the repression of immune response during infection, as well as this mechanism from the perspective of the pathogen, which pirates the host's lipoxygenase machinery to its own advantage as a probable immune-escape mechanism.

INNATE IMMUNITY AND PATHOGENS

It is well known that a series of pattern-recognition receptors is involved in the recognition of different microbial pathogens and induction of the innate response. Such receptors recognize distinct biochemical patterns of molecules displayed by the invading pathogen. The repertoire of innate immune receptors is very broad and includes several classes of germ-line–encoded proteins such as Toll-like receptors (TLRs), scavenger receptors, and C-type lectins. This wide array of recognition molecules allows the host to detect a variety of microbial molecules including carbohydrates, lipids, nucleic acids, and proteins [1, 2]. Distinct TLR ligands provide distinct activation status and cytokine production patterns for antigen-presenting cells (APCs), resulting in the induction of differential immune responses. Thus, TLRs are critical molecules to induce not only inflammatory responses but also fine-tune adaptive immune responses depending on invading pathogens [3]. TLRs activation can upregulate costimulatory molecules on APC, thus enhancing the activation of adaptive T-cell responses.