title: Elevated levels of circulating intercellular adhesion molecule-3 (cICAM-3) in Psoriasis.
abstract: Intercellular adhesion molecule (ICAM)-3 is important in regulating leukocyte function and T-lymphocyte-antigen presenting cell interactions. Soluble, circulating forms of ICAM-3 and ICAM-1 (cICAM-3, cICAM-1) exist in serum, and levels are elevated in a variety of autoimmune diseases. Two types of soluble circulating tumour necrosis factor receptor (cTNF-R1, cTNF-R2) are found in the sera of healthy people. cTNF-R1 binds TNF-alpha and is important in regulating TNF-alpha-mediated inflammation. Psoriasis is a T-lymphocyte-mediated disease, characterized by cutaneous expression of ICAM-1, ICAM-3 and TNF-alpha. As it is unknown whether cICAM-3 is increased in sera of patients with psoriasis, we measured serum levels of cICAM-3 and compared them to levels of cICAM-1, cTNF-R1 and clinical severity of psoriasis. Sera was taken from 112 healthy controls and 32 patients with psoriasis. Clinical severity of psoriasis was assessed using the psoriasis area severity index (PASI). cICAM-1, cICAM-3 and cTNF-R1 in serum were quantitated using a dual antibody, solid phase ELISA, Levels of cICAM-3, cICAM-1 and cTNF-R1 were significantly increased in sera of patients with psoriasis as compared with controls, and these elevated levels correlated with clinical severity of psoriasis as assessed by the PASI. Also, there were good correlations between serum levels of cICAM-3, cICAM-1 and cTNF-R1 in psoriasis. These results demonstrate, for the first time, that circulating levels of cICAM-3 are increased in psoriasis and that these levels correlate both with disease severity and with elevated levels of cICAM-1 and cTNF-R1. The exact physiologic roles of circulating, soluble adhesion molecules and cTNF-R1 are unknown, but it is hypothesised that elevation of their circulating levels, as observed in psoriasis, may play a role in modulating the inflammatory reactions occurring in this disease.
authors.affiliation: Section of Dermatology, University of Manchester, U.K.
authors.forename: C E
authors.initials: CE
authors.lastname: Griffiths
authors.forename: M J
authors.initials: MJ
authors.lastname: Boffa
authors.forename: W M
authors.initials: WM
authors.lastname: Gallatin
authors.forename: S
authors.initials: S
authors.lastname: Martin
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000378:metabolism; D000943:Antigens, Differentiation; D015815:Cell Adhesion Molecules / Q000097:blood*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D008297:Male; D008875:Middle Aged; D011565:Psoriasis / Q000097:blood* / Q000276:immunology / Q000503:physiopathology; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D015703:Antigens, CD; D000943:Antigens, Differentiation; D015815:Cell Adhesion Molecules; C483616:ICAM3 protein, human; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D018799:Intercellular Adhesion Molecule-1