Adhesion of splenocytes to brain microvascular endothelium in the BALB/c and SJL/j mouse systems

Adhesion of hematopoietic cells to endothelial (En) cells plays an important role in their migration into extravascular tissue. This report characterizes the adhesion properties of naive splenocytes to syngeneic and allogeneic mouse brain microvascular endothelium isolated from the BALB/c or SJL/j mouse strains. Syngeneic adhesion reaches maximum levels by 60 min at 37°C, but is more pronounced in the BALB/c system (mean adhesion = 10.7% ± 1.0) compared to adhesion seen in the SJL/j (mean adhesion = 4.3% ± 0.6). BALB/c, but not SJL/j adhesion, seems to be mediated, at least in part, by the interaction of CD11a/CD18 (lymphocyte function-associated antigen 1 (LFA-1)) with one of its ligands, because BALB/c adhesion is partially inhibited when the assay is carried out either in the presence of chelating agents or with antibodies to the CD11a/CD18 molecule. Activation of the endothelium with recombinant interferon-γ (rIFN-γ), recombinant interleukin-1α (rIL-1α), and recombinant tumor necrosis factor-α (rTNF-α), enhances adhesion in both BALB/c and SJL/j. IFN-γ and IL-1α mediated adhesion enhancement is abrogated by antibodies to the CD11a/CD18 molecules in the BALB/c but not in the SJL/j system. The adhesion of splenocytes to mouse brain En clearly has unique properties, and whether or not the differences seen in the SJL/j system in any way influences its susceptibility to the autoimmune demyelinating disease, experimental autoimmune encephalitis, remains to be determined.