Mls is not a single gene, allelic system. Different stimulatory Mls determinants are the products of at least two nonallelic, unlinked genes.

Abstract

Mls determinants share with MHC products the unique property of stimulating T cells at extraordinarily high precursor frequencies. The Mls system was originally described as a single locus on chromosome 1, with four alleles, Mlsa, Mlsb, Mlsc, and Mlsd, that encode polymorphic cell surface structures. However, the fundamental issues of polymorphism and allelism in the Mls system remain controversial. To clarify these questions, a formal segregation analysis of the genes encoding Mlsa and Mlsc determinants was carried out by testing the capacity of spleen cells from progeny of (Mlsa X Mlsc)F1 X Mlsb breedings to stimulate responses by unprimed T cells and by Mlsa- and Mlsc-specific cloned T cells. The results of this analysis indicated that the gene encoding Mlsa determinants is neither allelic to nor linked to the gene encoding Mlsc determinants. Together with previous findings, these results also suggest that another strongly stimulatory type, Mlsd, in fact results from the independent expression of unlinked Mlsa and Mlsc gene products. Based on these observations, it is concluded that, contrary to conventional concepts, the stimulatory phenotypes designated as Mlsa, Mlsc, and Mlsd can be accounted for by the independent expression of the products of at least two unlinked gene loci.

HLA-DQ? chain can present mouse endogenous provirus MTV-9 product and clonally delete Tcr V?5+ and V?11+ T cells in transgenic mice

“…We believe that such a system may exist. The reasons why it has not been identified could be because all major human class II molecules (DR, DQ, DP) can effectively present Mls-type antigens in regulating the T-cell repertoire and there are functionally redundant loci encoding human endogenous superantigens like Mls c in mouse (Abe et al 1987). Thus, there would be no "hole" in the system and differences in the self reacting T ceils cannot be identified between individuals.…”

T cell receptor-mediated recognition of self-ligand induces signaling in immature thymocytes before negative selection.

“…4). The binding of Mls ' § APC and the subsequent [Ca2+]i increase in Mls t' V~8.1 TG splenic T cells are strongly inhibited by anti-CD4 but minimally by anti-CD8, indicating a preferential role of CD4 molecules (24) in T cell Mls a recognition. Furthermore, splenic T cells are inhibited by mAb F23.1, reactive to the TG TCR, V~8.1, but not by F23.2, specific for V/~8.2.…”

“…T cell proliferation was assayed as described previously (24). Varying numbers of splenic T cells or thymocytes were cultured with 5 x 10 s B cells inactivated by 3,000-rad irradiation.…”

“…Each point represents the mean of pH]TdR incorporation of triplicate cultures. T cell proliferation was assayed as described previously (24).…”

Regulation of graft‐versus‐host‐reaction by Mlsa‐reactive donor T cells

“…In this model, injected A/J donor cells (MlsC) are exposed to alloantigens derived from the CBA/J parent, including both H-2Dk (class I) and Mlsd determinants. Because the designation Mlsd corresponds to coexpression of Mlsa and MlsC antigens [6], the A/J cells are exposed to Mlsa stimulation. No class I1 alloantigen would be encountered, since A/J and CBA/J strains are identical at class I1 loci.…”