Leukadherin-1 is an allosteric activator of CD11b/CD18. Increasing CD11b/CD18-dependent cell adhesion to fibrinogen, Decreasing leukocyte motility and transendothelial migration; reduces inflammation.

Leukadherin-1预处理减少了单核因子刺激的NK细胞分泌干扰素(IFN)-γ、肿瘤坏死因子(TNF)和巨噬细胞炎症蛋白(MIP)-1β。同时，它也降低了Toll样受体(TLR)-2和TLR-7/8刺激的单核细胞分泌IL-1β、IL-6和TNF的水平。Leukadherin-1调节NK细胞的细胞因子分泌，但不影响NK细胞中Syk激活[1]。LA1通过增加CD11b/CD18依赖的细胞与纤维蛋白原的粘附，其50%有效浓度(EC50，使粘附增加50%的有效浓度)为4μM[3]。

Leukadherin-1在多种动物模型中展现了强大的抗炎效果，包括自身免疫性肾炎模型，短期内未观察到明显副作用[1]。Leukadherin-1 (LA1) 增加白细胞附着，阻止它们的跨膜迁移和体内组织的招募。在完全MHC不匹配的原位肾移植小鼠模型中，LA1处理减少了异体移植物中间质白细胞的浸润，减少了新生内膜增厚和肾小球损伤，并将移植物存活率从CsA单用的48.5%提高到CsA与LA1联用时的100%（第60天）[2]。

NK cell stimuli (where used) were added as follows: (1) Syk inhibitor (1 μM), (2) Leukadherin-1 or dimethylsulphoxide (DMSO) (vector control) (7.5 μM). Shown to induce ∼82% of maximum response with negligible off-target effect, (3) anti-CD210 or isotype control (5 µg/ml), (4) 30-45 min after Leukadherin‐1 NK cells were stimulated with combinations of IL-12 (10 ng/ml), IL-15 (30 ng/ml) or IL-18 (10 ng/ml): either IL-12 + IL-15 or IL-12 + IL-18. Monocytes were stimulated using pam3csk4 (TLR-2 agonist, 300 ng/ml) or R848 (TLR-7/8 agonist, 2 µg/ml). Supernatants were stored at −80ºC for < 1 month before quantification. To exclude non-specific Leukadherin-1-mediated cytotoxicity, cell viability is assessed at 24 h using the CellTitre-Glo reagent. (Only for Reference)