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Diminished Proliferative Response of Con A‐blast Cells to Interleukin 2 in Adult Rats Exposed to Ethanol in Utero
Author(s) -
Norman D. C.,
Chang MP.,
Castle S. C.,
Zuylen J. E.,
Taylor A. N.
Publication year - 1989
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1989.tb00286.x
Subject(s) - in utero , concanavalin a , lymphoblast , immune system , immunity , cellular immunity , fetus , medicine , endocrinology , ethanol , interleukin 2 , fetal alcohol syndrome , splenocyte , andrology , biology , immunology , pregnancy , cell culture , in vitro , biochemistry , genetics
The fetal alcohol syndrome is associated with altered immunity. We attempted to delineate the mechanism of the decline in cell‐mediated immunity observed by others by using rats which were exposed to alcohol in utero and tested for immune integrity 3 months after birth. We found that concanavalin A‐stimulated T‐lymphoblast (Con A T‐blast) cells that were obtained from ethanol‐exposed rats had significantly diminished proliferative responses to both crude and recombinant intedeukin 2 compared to those obtained from normal and nutritional controls. The blunted response of Con A T‐blast cells to intedeukin 2 may be a biomarker of fetal exposure to alcohol.