High impact information on Ly6c

• Developmentally, CD4+CD8- thymocytes leave the thymus expressing low levels of Ly6C; 3 days later approximately 50% stably upregulate Ly6C without cell division or TCR engagement in the periphery [1].
• Our results show that the majority of primed CD8+ T cells generated in this system are not cycling and express increased levels of CD44 and Ly6C [2].
• Here we show that a significant fraction of these autoreactive cells in the normal adult thymus expresses NK1.1 and high levels of Ly-6C and also exhibits flexibility in MHC restriction [3].
• The murine alloantigen, Ly-6C, is found on 45% of bone marrow cells, 25% of splenocytes and 15% of lymph node cells in all inbred strains of mice tested, with the exception of NOD, NZB and ST [4].
• A recombination event in the 5' flanking region of the Ly-6C gene correlates with impaired expression in the NOD, NZB and ST strains of mice [4].

Biological context of Ly6c

• RESULTS: In IL-2-treated mice, donor CD8+ T cells persisted and developed a memory phenotype, based on CD44 and Ly6c expression at day 28, while mice given no IL-2 had fewer donor cells at all time points [5].
• Transfection of the Ly-6C genes from NOD and BALB/c into a murine carcinoma line indicates relative functional impairment of the NOD gene, thus paralleling performance in vivo [4].
• Southern blot analysis reveals a restriction fragment length polymorphism involving the Ly-6C gene which is unique to these three strains [4].
• Cloning of the affected genomic segment from the NOD mouse indicates the presence of an interruption in the flanking region of the Ly-6C gene at a point 475 bp upstream of the transcription initiation site and the consequent separation of distal 5' sequences from the body of the gene by at least 10 kb [4].
• Ly6C is a hemopoietic cell differentiation Ag found on a subset of CD8 T cells in the periphery [6].

Anatomical context of Ly6c

• In these three strains, Ly-6C expression can be detected on only 5% of bone marrow cells and not at all on cells from spleen or lymph node [4].
• Ly-6 superfamily members Ly-6A/E, Ly-6C, and Ly-6I recognize two potential ligands expressed by B lymphocytes [7].
• In the capillary flow-adhesion assay, Ly6C cross-linking significantly augments lymphocyte adhesion to endothelium, and this is inhibited by an Ab that blocks LFA-1 function [6].
• Primary osteoblasts and MC3T3 cells constitutively expressed both Ly-6A and Ly-6C antigens, although Ly-6C was much less abundant [8].
• Multiple expression of Ly-6C and accumulation of a Ly-6C pre-mRNA in activated macrophages involved in rejection of an allografted tumor [9].

Associations of Ly6c with chemical compounds

• Despite results indicating fewer disulfide constraints in the Ly-6C molecule, the predicted sequence contains 10 cysteine residues nearly perfectly matched with those predicted in Ly-6A [10].
• Moreover, they were not stimulated, in the presence of PMA, by doses of ionomycin that were optimal for normal T cells, but did respond to higher ionomycin concentrations (2 micrograms/ml), and this response was not altered by Ly-6C cross-linking [11].
• Using subtractive cDNA hybridization we have identified the cell surface protein Ly6C as differentially expressed on B cells stimulated with LPS only [12].

Regulatory relationships of Ly6c

• In vivo studies demonstrated that proinflammatory (Th1) cytokines transiently upregulate B cell Ly-6C expression [13].
• The abilities of Ly6C to induce LFA-1 clustering and to be re-expressed after signaling-associated down-regulation may be important in regulating the homing of CD8 T cells into lymph nodes and in subsequent steps of CD8 T cell activation and effector function that again involve LFA-1 [6].
• However, Ly-6I is also expressed on immature B cell populations that do not express Ly-6C [14].
• We compared Ly-6C expression on neutrophils and monocytes following short-term cell activation induced by C5a or phorbol esters or treatment with phosphatidylinositol-specific phospholipase-C (PI-PLC) [15].
• It was found that both Ly-6A/E and T cell-activating protein (TAP) molecules are markedly enhanced while Ly-6C is less affected [16].

Other interactions of Ly6c

• CH27 cells with low levels of Ly-6A/E ligand activity also lost expression of CD22, and cells transfected with CD22 gained the ability to bind the Ly-6A/E chimera and, to a lesser extent, the Ly-6C and Ly-6I chimeric proteins [7].
• For T lymphocytes from BALB/c (Ly-6.1) mice, Ly-6A/E, but not Ly-6C, molecules were synergistically induced by IFN-gamma and TNF [17].
• Although endogenous Ly-6A.2 and Ly-6C genes are IFN responsive, only the latter contains a clearly identifiable IFN responsive element [18].
• This renal expression and its interferon (IFN)-gamma inducibility in murine strains expressing different Ly-6 haplotypes were studied with monoclonal antibodies and cDNA probes that recognize Ly-6A/E and Ly-6C [19].
• Polyclonal B cell activators (anti-IgM and recombinant CD40 ligand trimer) showed minimal ability to independently induce Ly-6C expression on B cells but did enhance the ability of IFNs to induce expression [13].

Analytical, diagnostic and therapeutic context of Ly6c

• Two-dimensional immunoblotting revealed that Ly-6C of the Møs exists in multiple forms with a similar size but with different isoelectric points [9].
• In addition, the percentage of cells expressing Ly-6C increased among the CD8+ subset after anti-CD3 treatment and in the V beta 8+ CD8+ subset after treatment with SEB [20].
• Together, these observations suggest that the mechanisms leading to immunosuppression of DN T cells are complex and appear to involve abnormalities in signal transduction via the TCR and CD28 and possibly via Ly-6C and CD69 as well [21].
• Electron microscopic immunohistochemistry showed that the endothelial cells are the cell type expressing Ly-6C [22].
• The levels of surface Ly-6A/E and Ly-6C antigens were quantified by flow cytofluorometry [23].

References