Abnormal B lymphocyte development and autoimmunity in hypoxia-inducible factor 1α-deficient chimeric mice

Hidefumi Kojima, Hua Gu, Saeko Nomura, Charles C. Caldwell, Tetsuji Kobata, Peter Carmeliet, Gregg L. Semenza, Michail V. Sitkovsky

Research output: Contribution to journalArticle

Abstract

Immune cells are exposed to low oxygen tensions as they develop and migrate between blood and different tissues, but the mechanisms by which lymphocytes adapt to hypoxia are poorly understood. Studies reported here of hypoxia-inducible factor 1α (HIF1α) in lymphocyte development and functions suggest that it has a critical role in regulation of these processes. HIF-1α deficiency in Hif1α-/- → Rag2-/- chimeric mice results in dramatic and cell lineage-specific defects, which include appearance of abnormal peritoneal B-1-like lymphocytes, with high expression of B220 (CD45) receptor-associated protein tyrosine phosphatase and autoimmunity (accumulation of anti-dsDNA antibodies and rheumatoid factor in serum, deposits of IgG and IgM in kidney and proteinuria) as well as distortions of maturation of B-2 lymphocytes in bone marrow.

Original languageEnglish (US)
Pages (from-to)2170-2174
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume99
Issue number4
DOIs
StatePublished - Feb 19 2002

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