Figure 8.

T and B cell extracellular traps (TCETs and BCETs). Under certain experimental and pathophysiological conditions, ie stimulation with ionomycin or systemic lupus erythematosus patient serum, T cells can release ETs. A similar phenomenon was observed in CD8+ cells following the stimulation with anti-CD3/anti-CD28 antibodies, engaging T cell receptors. In presence of TGFβ and IL6, the naïve CD4+ T cells differentiate to the IL17 producing T cells (Th17 cells), which are associated with chronic inflammation and autoimmune diseases. In response to bacterial infection, this T cell population releases ETs, which are composed of DNA, histones and bactericidal proteins, leading to the entrapment of bacteria. Depending on the pathophysiological conditions Th17 cells can either promote or attenuate tumor development and metastasis. Further studies are required to understand whether cancer cells and tumor microenvironment may induce TET formation, which in turn can modulate tumor growth, metastasis and cancer immunity. B cells can release extracellular traps upon stimulation with PMA and ionomycin. BCETs were also observed after treatment with serum isolated from a systemic lupus erythematosus patient, indicating that soluble factors in the serum induce the DNA release and possibly BCETs could be involved in the pathogenesis of the disease. BCETs may serve as self-antigens that are recognized by other B cells, followed by autoantibody production and disease progression. Their role in cancer remains elusive.