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High concentration of adenosine in human visceral leishmaniasis despite increased ADA and decreased CD73
Author(s) -
RAI A. K.,
THAKUR C. P.,
VELPANDIAN T.,
SHARMA S. K.,
GHOSH B.,
MITRA D. K.
Publication year - 2011
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/j.1365-3024.2011.01315.x
Subject(s) - adenosine , adenosine deaminase , immune system , purinergic signalling , biology , extracellular , adenosine triphosphate , immunology , endogeny , 5' nucleotidase , enzyme , nucleotidase , catabolism , pharmacology , biochemistry , adenosine receptor , receptor , agonist
Summary Absence of an effective Th‐1 response has been demonstrated as a major cause for the disease pathology among patients with visceral leishmaniasis (VL). Defining strategies to prevent the development of Th‐2 response and/or initiate/activate effective Th‐1 response may be of help to reduce the growing incidence of drug unresponsiveness. Adenosine, which is considered as an endogenous anti‐inflammatory agent is generated in injured/inflamed tissues by the enzymatic catabolism of adenosine triphosphate (ATP), and it suppresses inflammatory responses of essentially all immune cells. The extracellular adenosine‐producing pathway comprises two major enzymes CD39 (ATP→ADP→AMP) and CD73 (AMP→Adenosine). In contrast, the adenosine‐degrading pathway contains only one major enzyme adenosine deaminase (ADA). Our study shows high concentration of adenosine in diseased condition, varying expression of enzyme involved in adenosine‐producing (CD73↓) and adenosine‐degrading (ADA↑) pathways. These are less studied in infections like VL but are very important in terms of endogenous regulation of immune response among patients.