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The Role of Adenosine-Producing Ectoenzymes in the Control of the Immune Homeostasis

Call for Papers

Adenosine (ADO) is a purine nucleoside that plays a key role in several biochemical processes, such as neuromodulation and vasodilation, energy transfer as adenosine triphosphate (ATP), and signal transduction as cyclic adenosine monophosphate (cAMP).

ADO and ATP play opposite roles in the control of immune response and inflammation. ATP is released by activated, stressed, or necrotic cells during inflammation and upon interaction with P2 purinergic receptors can activate chemotaxis of immune cells, production of reactive oxygen species by neutrophils, and release of proinflammatory cytokines by myeloid cells. In contrast, ADO, upon interaction with G protein coupled receptors, abrogates the function of T cells, NK cells, and macrophages, promotes the generation of tolerogenic antigen-presenting cells, and stimulates the generation and the activation of regulatory T cells and myeloid derived suppressor cells.

The extracellular balance between ATP and ADO is crucial during inflammatory response, since high levels of ATP are detected very early at the inflammatory site, whereas ADO is required to stop the inflammatory process. Ectoenzymes that are located on the cell surface have a key role in this process, since they exert their enzymatic activity in the extracellular compartment where they convert ATP to ADO. The “canonical” pathway involves an ectonucleoside triphosphate diphosphohydrolase-1 (ENTPD1/ CD39) that converts ATP to AMP. The “alternative” pathway includes an ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1/ CD203a or PC-1) that converts either ATP or ADPR (produced by ADP-ribosyl cyclase/CD38 from NAD+ ) to AMP. In both pathways, an ecto-5'-nucleotidase (CD73) converts AMP to ADO.

In the last years, the expression of ADO-producing ectoenzymes has been demonstrated on regulatory cell subsets and tumor cells. Moreover, several studies have addressed the role of these molecules in the onset of different human diseases. In particular, an increased expression and function of CD73 and CD39, as well as CD38, have been detected in different human tumors. On the other hand, a loss of the expression and function of these molecules has been demonstrated in patients with autoimmune/inflammatory diseases, where the control of the inflammatory and immune response results altered.

These novel studies clearly demonstrated the important role of ADO-producing ectoenzymes in the control of ATP/ADO extracellular balance that in turn can regulate the immune response and inflammation. Thus, we are interested in papers that explore novel aspects concerning the expression and function of CD38, CD39, CD73, and CD203a/PC-1 both in physiological and pathological conditions.

Potential topics include but are not limited to the following:

  • The expression of ectoenzymes in solid and hematological tumors and their role in the onset and progression of the disease
  • Altered expression of ectoenzymes in regulatory cell subsets during autoimmune/inflammatory diseases and possible correlations with disease progression and severity
  • The expression and function of ectoenzymes at the site of infection, in patients with infectious diseases (virus, bacteria, and other parasites)
  • Regulation of the expression and function of ectoenzymes by cytokines and/or other molecules
  • Novel mechanism of regulation of the immune response and inflammatory process performed by ADO-producing ectoenzymes
  • Presence of ectoenzymes on exosomes and/or microvesicles derived from tumor cells or regulatory cell subsets

Authors can submit their manuscripts through the Manuscript Tracking System at https://mts.hindawi.com/submit/journals/mi/ecih/.

Submission DeadlineFriday, 2 February 2018
Publication DateJune 2018

Papers are published upon acceptance, regardless of the Special Issue publication date.

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