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Regulation of Cysteine-Rich Intestinal Protein, a Zinc Finger Protein, by Mediators of the Immune Response
Robert J. Cousins and Lorraine Lanningham-Foster
The Journal of Infectious Diseases
Vol. 182, Supplement 1. A Workshop on Micronutrients and Infectious Diseases: Cellular and Molecular Immunomodulatory Mechanisms (Sep., 2000), pp. S81-S84
Published by: Oxford University Press
Stable URL: http://www.jstor.org/stable/30109335
Page Count: 4
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Cysteine-rich intestinal protein (CRIP), a member of the LIM protein family, has a unique double zinc finger motif as the defining feature. CRIP is highly expressed in intestine and immune cells. CRIP transgenic (Tg) mice and nontransgenic controls were challenged with lipopolysaccharide (LPS). Serum concentrations of interferon-γ and tumor necrosis factor-α were less while those of interleukin-α and -10 were greater in the Tg mice following LPS administration. CRIP-overexpressing splenocytes produce the same cytokine profile. These responses are consistent with a regulatory role for this protein in cell differentiation, which produces an imbalance in Thl and Th2 cytokines. Stimulation of CRIP protein levels by LPS is eliminated in metallothionein knockout mice, suggesting metallothionein is the source of zinc for this zinc finger protein and, further, that this could reflect a relationship to the zinc nutritional status and to the aberrant Th1/Th2 cytokine balance observed in zinc deficiency.
The Journal of Infectious Diseases © 2000 Oxford University Press