Journal
TOXICOLOGY AND APPLIED PHARMACOLOGY
Volume 165, Issue 3, Pages 227-236Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1006/taap.2000.8942
Keywords
aryl hydrocarbon receptor; 2,3,7,8-tetrachlorodibenzo-p-dioxin; B lymphopoiesis; chimeras; bone marrow
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Funding
- NIEHS NIH HHS [ES07216, ES04862, ES05774] Funding Source: Medline
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The ligand-activated aryl hydrocarbon receptor (AHR) is a cytosolic DNA binding protein. Although no biologic role for AHR has been elucidated, it mediates the immunotoxicity of xenobiotics such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), and its targeted inactivation produces abnormal immune system development. While investigators have demonstrated AHR's involvement in TCDD-induced B lymphocyte functional alterations, little is known about the receptor's possible role in early B cell maturation and whether exogenous ligands change this process. The purpose of this study was to determine, (1) whether bone marrow B lymphocyte maturation is affected by AHR presence, (2) if so, its relative importance in hematopoietic and/or nonhematopoietic elements and, (3) whether TCDD alters this process. Radiation chimeras were produced that were AHR positive (Ahr+/+) or negative (Ahr-/-) in either their nonhematopoietic or hematopoietic elements, or both. Marrow cells were analyzed for alterations in B lymphocyte maturation stage cell numbers in both vehicle- and TCDD-treated animals. Our results showed that (1) Ahr-/- animals had significantly higher numbers of pro/pre-B cells than Ahr+/+ animals, (2) TCDD treatment of Ahr+/+ animals produced a decrease in pro/pre-B cell numbers, whereas no effect was observed on Ahr-/- animals, and (3) AHR is required in both hematopoietic and stromal elements for maintenance of B cell subset maturation profiles. (C) 2000 Academic Press.
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