Expression and function of B7-1 (CD80) and B7-2 (CD86) on human epidermal Langerhans cells

• Published in: European journal of immunology Vol. 26; no. 2; p. 449
• Main Authors: Rattis, F M, Péguet-Navarro, J, Staquet, M J, Dezutter-Dambuyant, C, Courtellemont, P, Redziniak, G, Schmitt, D
• Format: Journal Article
• Language: English
• Published: Germany 01-02-1996
• Subjects: Antigen Presentation; Antigens, CD - biosynthesis; Antigens, CD - physiology; B7-1 Antigen - biosynthesis; B7-1 Antigen - physiology; B7-2 Antigen; Cell Separation; Cells, Cultured; Epidermis - immunology; Humans; Langerhans Cells - immunology; Langerhans Cells - metabolism; Membrane Glycoproteins - biosynthesis; Membrane Glycoproteins - physiology
• ISSN: 0014-2980
• DOI: 10.1002/eji.1830260227

In addition to T cell receptor triggering, activation of T cells requires costimulatory signals that have been shown to be mainly initiated through CD28. We analyzed the expression and function of the two ligands for CD28, B7-1 (CD80) and B7-2 (CD86), on human Langerhans cells (LC), the antigen-presenting cells from epidermis. Human LC freshly isolated from epidermis (fLC) expressed significant level of B7-2, which was increased upon a short culture in vitro. In contrast, B7-1 was undetectable on fLC but appeared at the cell surface after a 3-day culture in vitro. Pre-incubation of 18-h cultured LC with anti-B7-2 monoclonal antibodies (mAB) was sufficient to abrogate the binding of CTLA4-Ig fusion protein, while a combination of both mAB against B7-1 and B7-2 was necessary to obtain a complete inhibition of CTLA4-Ig binding on 3-day cultured LC, showing the absence of a third CTLA4 ligand. The function of B7-1 and B7-2 on human LC has been analyzed by adding mAb at the beginning of mixed epidermal cell lymphocyte reactions. Anti-B7-2 mAb and CTLA4-Ig, but not anti-B7-1 mAb, strongly inhibited allogenic. as well as recall antigen-induced T cell proliferation supported by fLC or 3-day cultured LC. Collectively, these results demonstrate that B7-2 is the major ligand for CD28/CTLA4 at the LC surface and that it plays a crucial role in human LC co-stimulatory function with little, if any, dependence of B7-1 expression.