Disease relevance of Ly6g

• LPS injection into copper-deficient mice resulted in a severe leukopenia but did not influence Ly-6G expression any more than did copper deficiency alone [1].

High impact information on Ly6g

• The phenotyping of rapidly recruited inflammatory leukocytes with 7/4 and Gr-1 monoclonal antibodies (mAbs) identifies 2 distinct populations, which we characterize as murine monocytes and neutrophils [2].
• Much larger proportions of bone marrow and peritoneal cells expressed Ly49B, all being CD11b(+) and comprising multiple subpopulations defined by light scatter, F4/80, and Gr1 expression [3].
• In addition, specific neutrophil depletion in vivo by low dose treatment with either of two Ly6G-specific mAb substantially decreased the relative CD8(+) T cell response against the nonsecreted, but not the secreted, Ag compared with control Ab-treated mice [4].
• Flow cytometry demonstrated that all peripheral blood EGFP+ cells were positive for CD2 and negative for the granulocyte Ag Ly 6-G (GR-1) [5].
• FACS analysis using 1A8 demonstrated that Ly-6G was expressed in bone marrow but not substantially on other lymphoid tissues, including activated T and B cells [6].

Biological context of Ly6g

• However, cells expressing the innate markers Gr-1 and CD11c were affected to a greater degree by increasing dose than lymphocytes of the adaptive immune response (Th1, CD4+, CD8+, CD19+), resulting in a change in the balance of innate and adaptive cell numbers to favor innate cells at higher infecting doses [7].
• Extensive studies in preclinical models indicate that these cells share the CD11b and the Gr-1 markers, possess a mixed mature-immature myeloid phenotype, and are responsible for the induction of T-cell dysfunctions, both tumor-specific and nonspecific [8].

Anatomical context of Ly6g

• At all time points, TNF mRNA colocalized with Mac-1-positive microglia/macrophages but not with Ly-6G (Gr-1)-positive polymorphonuclear leukocytes [9].
• In contrast, Ly-6c, CD44 and Gr-1 antigens were expressed on 51 +/- 6%, 85 +/- 9% and 37 +/- 5% of X-gal positive cells, indicating that X-gal positive cells were from macrophage or granulocyte lineages [10].
• Successful elimination of memory-type CD8+ T cell subsets by the administration of anti-Gr-1 monoclonal antibody in vivo [11].
• Immunosuppression during acute Trypanosoma cruzi infection: involvement of Ly6G (Gr1(+))CD11b(+ )immature myeloid suppressor cells [12].
• The results indicate the existence of an immunosuppressive mechanism during T. cruzi infection, mediated through IFN-gamma-dependent NO secretion by immature Ly-6G (Gr1)(+)CD11b(+ )myeloid cells [12].

Associations of Ly6g with chemical compounds

• GR-1hi expression (percentage of positive cells) and mean channel florescence were determined by FACScan analysis of a blood sample incubated with fluorescein isothiocyanate-anti-mouse Ly-6G (GR-1) [13].

Other interactions of Ly6g

• Intraperitoneal administration of anti-Gr-1 mAb caused almost complete elimination of Ly-6C(+) memory-type CD8(+) T cells as well as Ly-6G(+) granulocytes [11].
• Anti-Gr-1 mAb-treated mouse spleen cells exhibited greatly reduced IFN-gamma production in response to anti-CD3 mAb both in vitro and in vivo [11].

References