Anti-Mouse CCL5 Antibody (R6G9) is a neutralizing agent that binds to CCL5 to inhibit its chemotactic activity towards CD4 + T cells [1] [2].Anti-Mouse CCL5 Antibody (R6G9) does not suppress CD4 + T cell migration towards infection-derived liver cells, reduce CD4 + T cell hepatic accumulation, or impair CD4 + T cell migratory capacity [1].Anti-Mouse CCL5 Antibody (R6G9) serves as a tool to assess CCL5 ’s role in in vivo target cell killing by LCMV-specific CD8 + effector T cells [2].Anti-Mouse CCL5 Antibody (R6G9) can be used for the research of malaria infection and lymphocytic choriomeningitis virus infection [1] [2].
In Vivo, Anti-Mouse CCL5 Antibody (R6G9) (250 μg; i.p.; daily; 7 days starting day 7 post-infection) suppresses CD4+ T cell chemotaxis towards recombinant CCL5 but does not reduce CD4+ T cell accumulation in the liver or migration towards infection-derived liver cells in malaria-infected WSX-1-/- mice[1]. Anti-Mouse CCL5 Antibody (R6G9) (100 μg; i.v.; single dose) does not impair the in vivo killing activity of LCMV-specific CD8+ effector T cells[2].
In Vitro, Anti-Mouse CCL5 Antibody (R6G9) (10 µg/mL; 2 h pre-incubation) completely blocks the chemotactic response of CD4+ T cells from WSX-1-/- mice infected with Plasmodium berghei NK65 on day 14 to 100 ng/mL recombinant CCL5 in Transwell assays, but fails to inhibit their migration to infected liver tissues from mice in the same infection state[1]. Anti-Mouse CCL5 Antibody (R6G9) (0-60 min after peptide stimulation) enables quantitative detection of pre-stored CCL5 rapidly released by purified p14 effector T cells[2].
References:
[1]. Villegas-Mendez A, et al. WSX-1 signalling inhibits CD4⁺ T cell migration to the liver during malaria infection by repressing chemokine-independent pathways. PloS one. 2013;8(11):e78486.
[2]. Eberlein J, et al. Chemokine Signatures of Pathogen-Specific T Cells I: Effector T Cells. Journal of immunology (Baltimore, Md.: 1950). 2020 Oct 15;205(8):2169-2187.
In Vivo, Anti-Mouse CCL5 Antibody (R6G9) (250 μg; i.p.; daily; 7 days starting day 7 post-infection) suppresses CD4+ T cell chemotaxis towards recombinant CCL5 but does not reduce CD4+ T cell accumulation in the liver or migration towards infection-derived liver cells in malaria-infected WSX-1-/- mice[1]. Anti-Mouse CCL5 Antibody (R6G9) (100 μg; i.v.; single dose) does not impair the in vivo killing activity of LCMV-specific CD8+ effector T cells[2].
In Vitro, Anti-Mouse CCL5 Antibody (R6G9) (10 µg/mL; 2 h pre-incubation) completely blocks the chemotactic response of CD4+ T cells from WSX-1-/- mice infected with Plasmodium berghei NK65 on day 14 to 100 ng/mL recombinant CCL5 in Transwell assays, but fails to inhibit their migration to infected liver tissues from mice in the same infection state[1]. Anti-Mouse CCL5 Antibody (R6G9) (0-60 min after peptide stimulation) enables quantitative detection of pre-stored CCL5 rapidly released by purified p14 effector T cells[2].
References:
[1]. Villegas-Mendez A, et al. WSX-1 signalling inhibits CD4⁺ T cell migration to the liver during malaria infection by repressing chemokine-independent pathways. PloS one. 2013;8(11):e78486.
[2]. Eberlein J, et al. Chemokine Signatures of Pathogen-Specific T Cells I: Effector T Cells. Journal of immunology (Baltimore, Md.: 1950). 2020 Oct 15;205(8):2169-2187.