CD 54 (ICAM-1)

Accurate (1304.100.40), Biodesign (84H10, 15.2, MEM-111, MEM-112), Biogenesis (MEM-12), Biogenex (BBIG-1), Biosource (BC14, RR1-1), Caltag Laboratories (MEM111), Coulter (84H10), Dako (6.5B5), Exalpha Co. (D3.6), Immunotech (84H10), Novocastra (15.2), Pharmingen (3E2, HA58), Sanbio/Monosan (MEM-111), Serotec (84H10) and Zymed (MY13).

Apart from clone My13, which is applicable to both frozen and paraffin-embedded tissue sections, all the other antibodies are applicable to frozen sections only. In certain instances acetone fixation is recommended.

Cell-cell adhesion is critical in the generation of effective immune responses and is dependent upon the generation of a variety of cell surface receptors (Ohh & Takei, 1996). Intercellular adhesion molecule-1 (ICAM-1; CD 54) is an inducible cell surface glycoprotein expressed at a low level on a subpopulation of hematopoietic cells, vascular endothelium, fibroblasts and certain epithelial cells. However, its expression is dramatically increased at sites of inflammation, providing important means of regulating cell-cell interactions and hence inflammatory responses. ICAM-1 is induced by proinflammatory cytokines such as interleukin-1, tumor necrosis factor-a or interferon-g (Stratowa & Audette, 1995). The CD 54 antigen (ICAM-1) is a 90 kD integral membrane glycoprotein with seven potential N-linked glycosylation sites.

The CD 54 antigen is expressed on monocytes and endothelial cells. It is also a lymphokine-inducible molecule and has been shown to be a ligand for LFA-1-mediated adhesion. Expression of the antigen can be induced or upregulated on many cell types including B and T lymphocytes, thymocytes, fibroblasts, keratinocytes and epithelial cells. In its function of mediating immune and inflammatory responses, CD 54 antigen mediates adhesion of T-cells with antigen presenting cells and is involved in T-cell to T-cell and T-cell to B cell interactions (for review, see Fleming, 1990, 1991).
Increased expression of ICAM-1 has been associated with many types of atherosclerotic lesions (Poston et al, 1992). In rejecting kidneys the antibody highlights all infiltrating cells strongly as well as glomerulus epithelium, endothelium on capillaries, vessels and mesangium (Knapp et al, 1989).

•Fleming S 1990. Cellular functions of adhesion molecules, (editorial). Journal of Pathology 161: 189-190.

•Fleming S 1991. Cell adhesion and focusing of inflammatory responses (commentary) Histopathology 19: 571-573.

•Knapp W, Dorken B, Gilks WR et al (eds) 1989. Leucocyte typing IV. White cell differentiation antigens. Oxford: Oxford University Press.

•Ohh M, Takei F 1996. New insights into the regulation of ICAM-1 gene expression. Leukemia and Lymphoma 20:223-228.

•Poston RN, Haskard DO, Coucher JR et al 1992. Expression of intercellular adhesion molecule-1 atherosclerotic plaques. American Journal of Pathology 140: 665-673. atherosclerotic plaques. American Journal of Pathology 140: 665-673.

•Stratowa C, Audette M 1995. Transcriptional regulation of the human intercellular adhesion molecule-1 gene: a short overview. Immunobiology 193:293-304.

Manual of diagnostic antibodies for immunohistology / Anthony S.-Y. Leong, Kumarasen Cooper, F. Joel W.-M. Leong.