Lack of mature B cells in nude mice with X-linked immune deficiency.

Abstract

Mice were bred that simultaneously expressed the mutations nude and x-linked immune deficiency (xid). These doubly deficient animals had less than 10% of normal serum immunoglobulin levels. Their spleen cells did not respond to thymus-independent antigens in vitro nor did they respond to lipopolysaccharide. There was a virtual absence of cells with surface mu, kappa, or lambda 1, as detected by fluorescence. Sections of lymphoid organs revealed an absence of primary B cell follicles. Taken together, these results indicate a lack of mature B cells in nude xid mice. The possibility is considered that mature B cells belong to two subpopulations representing two lineages, one controlled by alleles at the xid locus and the other by alleles at the nude locus.

Reconstitution of immunodeficient SCID/beige mice with human cells: Applications in preclinical studies

“…This defect corresponds to Bruton's agammaglobulinemia in humans. Crosses with nude mice have been made in order to obtain mice with both T and B cell deficiency (Wortis et al, 1982). Mice with severe combined immunodeficiency (SCID) have a mutation in a gene responsible for DNA repair; recombination of VDJ (variable, diversity and joining) segments necessary for the generation of T and B cell receptors is thus severely inhibited (Bosma et al, 1983).…”

CD4+ T Cells and CD40 Participate in Selection and Homeostasis of Peripheral B Cells

“…Mice with defects in both Bruton's tyrosine kinase (Btk, a key BCR signaling protein) and CD40 have a profound reduction in peripheral B cell numbers compared with mice with either defect alone (24,25), implying CD40 promotes survival in the absence of sufficient BCR signals. Additional studies have demonstrated altered V H gene usage in athymic mice (26), reduced transitional cell maturation in athymic rats (27), impaired B cell development in Btk mutant nude mice (28)(29)(30), inability to mediate chronic graft versus host disease when B cells develop in the absence of CD4 T cells (31), increased autoreactivity of mature B cells from CD40L-deficient patients (32), and impaired B cell maturation in humanized mice lacking T cells (33).…”

Development of Ly-1+ B cells in immunodeficient CBA/N mice.

“…Novel formulations of B cell development pathways should take into consideration present evidence for interplay among T and B lymphocyte subpopulations within the two lineages of differentiation (10)(11)(12). Besides, the differentiation of common B cell precursors in CBA/N mice shows a strong T cell dependence (13)(14)(15). Thus, in addition to the defects of the major subpopulation I spontaneously caused by xid genes (3), the alterations in intrathymic development present in CsX-CBA/N and transferred mice (7) may contribute to the paucity of B cells observed in the major (Ly-1 -) lineage.…”