title: CD43 deficiency has no impact in competitive in vivo assays of neutrophil or activated T cell recruitment efficiency.
abstract: Using noncompetitive methodologies comparing CD43(+/+) and CD43(-/-) mice, it has been reported that CD43(-/-) leukocytes exhibit reduced recruitment efficiency to sites of inflammation. More recent analyses demonstrate that CD43 on activated T cells can function as an E-selectin ligand (E-SelL) in vitro, suggesting that CD43 might promote rolling interactions during recruitment of leukocytes and account for the reported recruitment deficits in CD43(-/-) T cells and neutrophils in vivo. Internally controlled competitive in vivo methods using fluorescent tracking dyes were applied to compare recruitment efficiency of CD43(+/+) vs CD43(-/-) activated T cells to inflamed skin and of peripheral blood neutrophils to inflamed peritoneum. A simple CFSE perfusion method was developed to distinguish arterial/venous vasculature and confirm appropriate extravasation through venules in a Con A-induced cutaneous inflammation model. In vivo recruitment of peripheral blood neutrophils to inflamed peritoneum was core 2 GlcNAcT-I dependent, but recruitment efficiency was not influenced by absence of CD43. There were also no significant differences in core 2 GlcNAcT-I-dependent, selectin-dependent, cutaneous recruitment of activated T cells from CD43(+/+) and congenic CD43(-/-) mice in either B6 or P-selectin(-/-) recipients despite biochemical confirmation that a CD43-specific E-SelL was present on activated T cells. We conclude that recruitment of neutrophils and activated T cells in these in vivo models is not influenced by CD43 expression and that if CD43 on activated T cells performs an E-SelL function in vivo, it contributes in a limited physiological context.
authors.affiliation: Biomedical Research Centre and Department of Pathology and Laboratory Medicine, University of British Columbia, 2222 Health Sciences Mall, Vancouver, British Columbia, Canada V6T 1Z3. doug@brc.ubc.ca
authors.forename: Douglas A
authors.initials: DA
authors.lastname: Carlow
authors.forename: Hermann J
authors.initials: HJ
authors.lastname: Ziltener
mesh_terms: D000818:Animals; D001681:Biological Assay; D003872:Dermatitis / Q000276:immunology*; D005452:Fluoresceins / Q000032:analysis / Q000378:metabolism; D036904:Leukocyte Rolling / Q000235:genetics; D051917:Leukosialin / Q000032:analysis / Q000235:genetics / Q000378:metabolism*; D008213:Lymphocyte Activation / Q000235:genetics; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D017351:N-Acetylglucosaminyltransferases; D009504:Neutrophils / Q000737:chemistry / Q000276:immunology*; D010537:Peritoneum / Q000098:blood supply; D010538:Peritonitis / Q000276:immunology*; D017468:Receptors, Fibroblast Growth Factor / Q000032:analysis / Q000276:immunology; D012795:Sialoglycoproteins / Q000032:analysis / Q000276:immunology; D012867:Skin / Q000098:blood supply; D013388:Succinimides / Q000032:analysis / Q000378:metabolism; D013601:T-Lymphocytes / Q000737:chemistry / Q000276:immunology*; D014699:Venules / Q000166:cytology / Q000276:immunology
chemical_list: C087165:5-(6)-carboxyfluorescein diacetate succinimidyl ester; D005452:Fluoresceins; D051917:Leukosialin; D017468:Receptors, Fibroblast Growth Factor; D012795:Sialoglycoproteins; D013388:Succinimides; C086711:cysteine-rich fibroblast growth factor receptor; D017351:N-Acetylglucosaminyltransferases; C053024:beta-1,3-galactosyl-O-glycosyl-glycoprotein beta-1,6-acetylglucosaminyl transferase