The recently detected T axis differentiation antigen, which was provisionally designated as T-lymphocyte-macrophage-associated antigen (TLMA) could now be identified as the neutral glycosphingolipid GgOse4Cer (asialo-GM1). TLMA is not only expressed on lymphocytes on the T lineage and on macrophages of the rat, but also on eosinophilic cells. On erythrocytes, the determinants are only detectable after neuraminidase treatment. Within the cell surface of thymic lymphocytes, the antigen determinant is partly masked by sialic acid residues. Presently, it cannot be decided whether the masking effect is brought about by sialic acid residues of adjacent glycolipid molecules or whether a nonreactive sialylated precursor molecule exists.

SummaryInfection of sensitive adult mice with myeloproliferative sarcoma virus (MPSV) results in a myeloproliferative syndrome. Two components of the viral genome are required to induce this unique pathology: the mos oncogene and sequences within the U3 region of the long terminal repeat (LTR). In studies designed to identify the target cell of MPSV and thus better understand the mechanism by which a myeloproliferative syndrome is induced, we have infected a series of T cell lines with MPSVbased vectors . The results presented here show that infection with neon MPSV abrogates the requirement for an antigen-specific or feeder cell-dependent stimulation, without altering the requirement for interleukin 2. Significantly, this response is not dependent on the mos oncogene, but requires sequences within the U3 region of the MPSV LTR . No alteration in the constitutive or induced levels of lymphokines released by these cells was observed. These results suggest a model in which T cells acquire a proliferative advantage by uncoupling the proliferative response from the lymphokine synthesis that is induced by activation of the T cell receptor. These cells are thus poised for antigen stimulation and secretion ofcytokines that stimulate myelopoiesis.