Faculty Research 1980 - 1989


Phenotypic, functional, and molecular genetic comparisons of the abnormal lymphoid cells of C3H-lpr/lpr and C3H-gld/gld mice.

Document Type


Publication Date



Cell-Differentiation, Cell-Separation, Comparative-Study, DNA: an, Leukemia-Experimental: mi, Lymph-Nodes: im, pa, Lymphoproliferative-Disorders: fg, im, Mice, Mice-Inbred-BALB-C, Mice-Inbred-C3H, Mice-Inbred-C57BL, Mice-Mutant-Strains, Mouse-Leukemia-Viruses, Nucleic-Acid-Hybridization, Phenotype, SUPPORT-U-S-GOVT-P-H-S, T-Lymphocytes: cl, me, pa

JAX Location

JAX VOL 1986

JAX Source

J-Immunol. 1986 Jun 1; 136(11):4075-84.


AI19010, CA31102


Lymph node cells from C3H mice homozygous for lpr and gld were compared for expression of cell surface antigens, lectin-binding sites, functional characteristics, expression of ecotropic MuLV, and organization of Ig and T cell receptor (TcR) beta-chain genes. The abnormal cells (Ly-2-/L3T4-) populating nodes of both mutant strains were specifically purified by using plate separation techniques. The purified abnormal cells were shown to express the beta-chain of the TcR, to exhibit rearrangements of the beta-chain genes, and to express TcR beta and alpha gene mRNA, demonstrating the T cell origin of these populations. FMF analyses of the separated abnormal cells showed them to be Thy-1+, Ly-1+, Ly-2-, L3T4-, Ly-5(B220)+, Ly-6+, Ly-22+, Ly-24+, sIg-, ThB-, Ia-, HSA-/+, and PC.1+ and to bind at high levels lectins that normally bind preferentially to B cells. These cells did not proliferate or generate CTL in response to stimulation with alloantigens, and supernatants of cells stimulated with Con A were devoid of IL 2. These characteristics do not correspond to those of any known immature or mature population of normal T cells. The findings that the abnormal T cells of lpr and gld homozygotes are indistinguishable for each parameter examined support the suggestion that these mutations may affect different enzymes in a common metabolic pathway of major importance to T cell differentiation and function.

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