Transfer of bone marrow (BM) from autoimmunity‐prone mice homozygous for the new lymphoproliferation mutation (lpr^cg) caused systemic lymphoproliferation in irradiated lpr^cg/lpr^cg recipients but not in irradiated +/+ recipient (J. Exp. Med. 1990. 171: 519; Eur. J. Immunol. 1991. 21: 63). It was thus hypothesized that the lpr^cg gene expresses its function at lymph nodes (LN) to provide anomalous lpr^cg/lpr^cg lymphoid cells with the environment where they can accumulate. This was confirmed by LN transplantation and BM transfer studies. In the LN transplantation study lp^cg/lpr^cg LN grafts with or without in vitro irradiation swelled and lpr^cg/+ LN grafts were slightly hyperplastic or apparently normal; however, whereas +/+ LN grafts atrophied in lpr^cg/lpr^cg recipients, they were all histologically normal in +/+ and lpr^cg/+ recipients. Irradiation of lpr^cg/lprc^cg LN grafts significantly retarded their swelling in lpr^cg/lpr^cg recipients. In the BM transfer study lpr^cg/lpr^cg BM cells caused systemic lymphoproliferation in lpr/lpr and gld/+, lpr^cg/+ recipients and sporadic LN swelling in lpr^cg/+ recipients but LN atrophy in gld/gld recipients. In the study using both techniques in combination, lpr/lpr LN grafts swelled but gld/gld LN grafts atrophied in lpr^cg/lpr^cg BM → +/+ chimeras. All the swollen LN contained Thy‐1⁺CD4⁻CD8⁻ lymphoid cells or “double‐negative (DN)” T cells characteristic of the lpr disease. Analysis of DNA restriction fragment length polymorphism demonstrated that lpr^cg/lpr^cg DN cells derived from lpr^cg/lpr^cg BM cells accumulated in lpr/lpr LN and gld/+, lpr^cg+ LN. The following conclusions have been drawn: (a) the lpr^cg gene determines the ability of lpr^cg/lpr^cg DN cell to accumulate in LN; (b) this genetic trait is not totally recessive differing from lymphoproliferation; (c) lpr/lpr LN and gld/+, lpr^cg/+ LN are equivalent to lpr^cg/lpr^cg LN in the receptivity of lpr^cg/lpr^cg DN cell accumulation thus supporting the allelism of lpr with lpr^cg and the complementation between gld and lpr^cg (J. Exp. Med. 1990. 171: 519), respectively; (d) the ability of lpr^cg/lpr^cg LN to accumulate DN cells is partially resistant to irradiation; (e) lpr^cg/lpr^cg DN cells may cause atrophy of gld/gld LN and +/+ LN and (f) the gld and lpr genes are different from each other in the phenotype expressed at the LN site.