Recombinant Mouse ALCAM Fc Chimera Protein, CF

ALCAM (activated leukocyte cell adhesion molecule), designated CD166 and also called MEMD and SC‑1/DM‑GRASP/BEN in the chicken, is a 100 ‑ 110 kDa type I transmembrane glycoprotein and a member of the Ig CAM family within the immunoglobulin superfamily (1). ALCAM is expressed on thymic epithelium, microvascular endothelium, activated lymphocytes and monocytes, and monocyte‑derived dendritic cells (1, 2). Mouse ALCAM cDNA encodes 583 amino acid (aa), including signal peptide (27 aa), extracellular domain (ECD, 500 aa) with two V‑type and three C2‑type Ig‑like domains, transmembrane (22  aa) and cytoplasmic (34 aa) domains (1). Mouse ALCAM ECD shares 98%, 93% and 92% aa sequence identity with rat, human/porcine and bovine/equine ALCAM, respectively. A secreted isoform in endothelial cells that is truncated at aa 133 (sALCAM) antagonizes full‑length ALCAM (3, 4). ALCAM mediates low‑affinity adhesion with itself or the cysteine‑rich scavenger receptor CD6 to regulate T cell development, immunological synapses (IS), and cell migration through endothelial junctions (1 ‑ 11). ALCAM on thymic epithelia mediates adhesion to CD6 on CD4⁺CD8⁺ T cells (6). Adhesion of ALCAM‑expressing antigen presenting cells and CD6‑expressing T cells stabilizes the early IS, while later it enhances CD3 effects on T cell proliferation, CD25 expression, and Th1 commitment (2, 7, 8). High ALCAM expression at the blood‑brain barrier in active multiple sclerosis, and its mouse model (EAE), promotes leukocyte migration to the brain (8, 9). High ALCAM expression on human melanoma cell lines appears to be pro‑metastatic, but anti‑metastatic activity has been reported in human breast cancer (3, 10, 11). ALCAM may influence expression or adhesion of the neuronal adhesion molecule NCAM‑L1, both in the developing retina and invasive melanoma (3, 12).