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On the expression of nitric oxide synthase by human macrophages. Why no NO?
Author(s) -
Albina Jorge E.
Publication year - 1995
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.58.6.643
Subject(s) - nitric oxide , biology , macrophage , nitric oxide synthase , mediator , microbiology and biotechnology , effector , function (biology) , monocyte , downregulation and upregulation , immunology , in vitro , biochemistry , gene , endocrinology
The production of nitric oxide (NO) and its role in the anti‐tumor and anti‐microbial effects of rodent macrophages appears well established. In contrast, the circumstances required for its release from human monocytes/macrophages and its potential role in human pathology remain controversial. Evidence to be discussed suggests that NO is a redundant, autotoxic, immunosuppressive, and inefficient mediator of macrophage function. For these reasons, the expression of nitric oxide synthase as a rapid‐response, high‐output effector pathway may have been evolved out of the human monocyte/macrophage response repertoire or severely restricted in its expression. Hypothetical roles for a modest and circumscribed production of NO by human macrophages are proposed.