A new lymphocyte cell surface antigen, Ly-22.2, controlled by a locus on chromosome 4 and a second unlinked locus.

A serum raised by immunizing (B10.A(4R) X B10.HTT)F1 mice against A.AL lymphocytes detects a new antigenic determinant designated Ly-22.2. Ly-22.2 expression is under the control of two independently segregating genes, one of which maps to chromosome 4 adjacent to a locus affecting XenCSA expression. Ly-22.2 is present in varying amounts in all lymphoid organs, but appears to be expressed primarily on T lymphocytes. Ly-22.2 is not detectable in brain, kidney, lung, liver, or erythrocytes. Strain distribution studies show Ly-22.2 is present in all strains examined except B10-derived congenic strains. It is of interest that C57BL/6 and C57BL/10 mice differ in the expression of this antigen.

Genetics of susceptibility for radiation-induced leukemia. Mapping of genes involved to chromosomes 1, 2, and 4, and implications for a viral etiology in the disease.

Susceptibility to radiation-induced leukemia in (A/J x B10)F2 mice is encoded for by genes in chromosomes 1, 2, and 4. The loci involved in chromosomes 1 and 4 are close to or similar to xenotropic virus inducibility locus on chromosome 1 and a locus-affecting expression of xenotropic MuLV envelope-related cell surface antigens. Radiation-induced leukemia-1 (Ril-1) on chromosome 2 plays an overriding influence in susceptibility to the disease. This locus might encode ecotropic viral-associated genetic information or might contain cellular sequences with oncogenic potential. These findings are of interest in view of the importance of recombinant viruses to leukemogenesis. Furthermore, it is intriguing that Ril-1 is located in a chromosomal site rich in thymus differentiation-specific loci. An explanation for tissue-specific activation of endogenous viruses is that activation of the virus in question is dependent on differentiation-specific steps.

Functional properties of Ly 11.2 lymphocytes: a role for these cells in leukemia?

Functional studies of lymphocyte subpopulations reveal that Ly 11.2, a newly defined T cell surface antigen, is present on prothymocytes and natural killer cells, but not on suppressor T cells for antigen-specific IgE antibody responses, Ly 1+, 2-, 3- helper T cells nor on tumor-specific cytotoxic effector cells. Changes in the expression of Ly 11.2 regularly accompany leukemogenesis and are quite distinct from changes of other cell surface antigens thus far observed. After intrathymic inoculation of radiation leukemia virus (RadLV), many more Ly 11.2-positive cells are found expressing viral antigens than cells expressing other cell surface phenotypes. In addition, after RadLV inoculation, significantly more Ly 11.2-positive cells can be found in the thymus of susceptible mice than in the thymus of resistant mice. The greater availability of permissive (Ly 11.2-positive) cells in susceptible vs resistant hosts at the time when infectious virus is present may account for the shorter latency period and high leukemia incidence of susceptible vs resistant mice.

Definition of a new T lymphocyte cell surface antigen, Ly 11.2.

The present communication defines a new cell surface antigen, Ly 11.2, which appears from its strain and tissue distribution to be distinct from all other previously defined normal or virally coded antigens or traits of the mouse. Lymphocytes of the T cell lineage, but not B cells or nonlymphoid cells, bear this marker. Although the locus coding for this antigen appears to be closely linked to the minor histocompatibility locus H-30 and to the locus coding for Ly 6.2, a chromosome assignment has not yet been made for my of these loci.

In vivo or in vitro treatments with anti-I-J alloantisera abolish immunity to AKR leukemia.

This paper provides evidence for the involvement of immune mechanisms in conferring resistance to a spontaneous AKR leukemia. It is shown that genes in the B, J, or E subregions of the H-2 complex confer resistance to a spontaneously arisen, tissue culture-adapted AKR thymoma, BW5147. A direct correlation is demonstrated between survival to injected BW5147 cells and humoral responsiveness in various hybrids obtained from crosses of AKR mice and C57BL/10 or C3H/DiSn derived congeneic strains differing at H-2. Cellular immunity appears to play no role in resistance to the proliferation of tumor cells. It is further established that development of effective humoral immunity depends on B cells and Ly-1+, 2-, 3- helper T-cells bearing the I-Jk phenotype. These findings seem directly applicable to the spontaneous disease, and results of studies using transformed cells from an overtly leukemic AKR mouse parallel those obtained using BW1547 cells.