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NF-B RelA-deficient Lymphocytes: Normal Development of T Cells and B Cells, Impaired Production of IgA and IgG1 and Reduced Proliferative Responses

Takahiro S. Doi^*, Toshitada Takahashi^*, Osamu Taguchi, Takachika Azuma, and Yuichi Obata^*

From the ^* Laboratory of Immunology and the Laboratory of Experimental Pathology, Aichi Cancer Center Research Institute, Chikusa-ku, Nagoya 464; and the Research Institute for Biological Sciences, Science University of Tokyo, Noda 278, Japan

To investigate the function of NF-B RelA (p65), we generated mice deficient in this NF-B family member by homologous recombination. Mice lacking RelA showed liver degeneration and died around embryonic day 14.5. To elucidate the role of RelA in lymphocyte development and function, we transplanted fetal liver cells of 13.5-day embryos from heterozygote matings into irradiated SCID mice. Within 4 weeks, both T and B cells had developed in the SCID mice receiving relA–/– fetal liver transplants, similar to the relA+/+ and +/– cases. T cells were found to mature to Thy-1⁺/TCRβ⁺/CD3⁺/CD4⁺ or CD8⁺, while B cells had the ability to differentiate to IgM⁺/B220⁺ and to secrete immunoglobulins. However, the secretion of IgG1 and IgA was reduced in RelA-deficient B cells. Furthermore, both T and B cells lacking RelA showed marked reduction in proliferative responses to stimulation with Con A, anti-CD3, anti-CD3+anti-CD28, LPS, anti-IgM, and PMA+calcium ionophore. The results indicate that RelA plays a critical role in production of specific Ig isotypes and also in signal transduction pathways for lymphocyte proliferation.

¹Abbreviations used in this paper: ABC, avidin-biotin enzyme complex; B6, C57BL/6; ED, embryonic day; ES, embryonic stem; HE, hematoxylineosin; HSV-tk, herpes simplex virus-thymidine kinase; MCH, Jcl: MCH(ICR); TUNEL, TdT-mediated dUTP nick end labeling.

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