Leukocyte cell-derived chemotaxin-2 (LECT2) is a protein first described in 1996 as a chemotactic factor for neutrophils, i.e. it stimulated human neutrophils to move directionally in an in vitro assay system. The protein was detected in and purified from cultures of Phytohaemagglutinin-activated human T-cell leukemia SKW-3 cells.[5] Subsequent studies have defined LECT2 as a hepatokine, i.e. a substance made and released into the circulation by liver hepatocyte cells that regulates the function of other cells: it is a hepatocyte-derived, hormone-like, signaling protein.[6][7]
LECT2 has been detected in the blood and other tissues in a wide range of animal species from zebrafish to man. Furthermore, its levels in these tissues often change as a function of various diseases. These findings indicate that LECT is an evolutionary conserved protein, has one or more important functions, and may be involved in various diseases. However, LECT2's relationships to these diseases requires much further study before they can be regarded as established and clinically useful. One exception to this, however, is its proven role in amyloidosis. LECT2 is one of the more common causes of systemic (as opposed to localized) amyloidosis in North America as well as certain other ethnically-rich locations.[8]
LECT2 and its gene, LECT2, are currently areas of active research that seek to implicate them as contributors to, markers for the presence of, and/or prognostic indicators for the severity of not only amyloidosis but also osteoarthritis, rheumatoid arthritis, and other types of inflammation-related disorders; the metabolic syndrome and diabetes; and various types of liver disease.[6]
