Extracellular Traps and Co-Stimulatory Molecules in Leukocytes of Patients with Positive Serology for Chagas Disease

Extracellular traps (ETs) are structures composed of chromatin, histones and granular proteins, first described on 2004 in neutrophils by Brinkmann, et al. [1], constitute a new mechanism of defense of the immune system in response to diverse microorganisms and other varied stimuli. In stimulated cells, the development of this phenomenon begins with the decondensation of the chromatin simultaneously with the loss of the nuclear structure. As the nuclear sheaths are separated, cytoplasm and granules are shown unchanged. At a later time the nuclear membrane disintegrates into vesicles and the granules disintegrate, resulting in the mixing of the contents of the nuclear, cytoplasmic and granular compartments. Finally, the combination of all these components is thrown into the extracellular space [2]. The most studied costimulatory pathway in T lymphocyte activation is the B7-1 (CD80)/B7-2 (CD86): CD28/CTLA4 pathway. Regulatory T lymphocytes are dependent for their generation and maintenance of costimulation by this B7: CD28 pathway [3]. The co-stimulatory molecules CD80 and CD86 are constitutively expressed in some cell types and are classically described as molecules of professional antigen-presenting cells such as dendritic cells, macrophages and B lymphocytes. These molecules are expressed at low intensity in resting cells but can be induced by inflammatory cytokines and by stimulation of Toll-like receptors with microbial products such as lipopolysaccharide (LPS) [3]. In neutrophils, it has been observed that such costimulatory molecules can be stored in their cytoplasmic granules and under certain stimuli expressed on the cell surface [4]. In a previous work, we have described the Colocalization of CD80 and CD86 costimulatory molecules in neutrophil extracellular traps (NETs) in cultures of total autologous leukocytes in healthy human blood samples [5].