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Blood, 15 September 2005, Vol. 106, No. 6, pp. 2069-2075.
Prepublished online as a Blood First Edition Paper on June 7, 2005; DOI 10.1182/blood-2004-07-2731.
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IMMUNOBIOLOGY
Impaired Ig class switch in mice deficient for the X-linked lymphoproliferative disease gene Sap
Umaima Al-Alem,
Cuiling Li,
Nathalie Forey,
Francis Relouzat,
Marie-Claude Fondanèche,
Sean V. Tavtigian,
Zhao-Qi Wang,
Sylvain Latour, and
Luo Yin
From the International Agency for Research on Cancer, Lyon, France; the Division of Pulmonary, Allergy, and Critical Care Medicine, Columbia University, New York, NY; and the Unité INSERM 429, Hôpital Necker-Enfants Malades, Paris, France.
X-linked lymphoproliferative disease (XLP) is characterized by abnormal immune responses to Epstein-Barr virus attributed to inactivating mutations of the SAP gene. Previous studies showed immunoglobulin E (IgE) deficiency and low serum IgG levels in Sap-deficient mice before and after viral infections, which are associated with impaired CD4+ T-helper function. In the present work, we find that signaling lymphocytic activation molecule (SLAM)-associated protein (SAP) is expressed in B cells and this expression is down-regulated after stimulation with lipopolysaccharide (LPS) and interleukin 4 (IL-4). We demonstrate that B cells from Sap-deficient mice exhibit reduced IgG and IgA production in vitro. This impairment correlates with decreased circular transcript levels of I , I 2a, I2b, and I3 after stimulation, which indicate a defective Ig switch recombination in Sap-deficient B cells. While XLP is believed to cause defects in T, natural killer T (NKT), and natural killer (NK) cells, our results indicate that B cells are also affected. (Blood. 2005;106:2069-2075)
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