PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 10644023-5 2000 After iontophoresis with nickel sulfate, only individuals sensitized to nickel reacted with a positive clinical response, increase in cutaneous blood flow, decline in epidermal CD-1a-positive cells, increase in epidermal proliferation (Ki-67-positive cells), pronounced infiltration of cells positive for CD4, CD11, or CLA, and cellular activation (expression of ICAM1, HLA-DR). Nickel 25-31 intercellular adhesion molecule 1 Homo sapiens 363-368 19844976-5 2010 Our results indicate that soluble cobalt, nickel, and molybdenum can induce monocyte up-regulation of T cell costimulatory molecules (CD80, CD86, ICAM-1) in human monocytes/macrophages. Nickel 42-48 intercellular adhesion molecule 1 Homo sapiens 146-152 7864660-3 1994 Our aim was to assess the effects of sensitizing metal haptens (nickel, cobalt and chromium) compared with the toxic metal cadmium on the induction of ICAM-1 and the production of TNF alpha by epidermal cells. Nickel 64-70 intercellular adhesion molecule 1 Homo sapiens 151-157 7864660-5 1994 Using FACS analysis, ICAM-1 expression was found to be induced only by nickel. Nickel 71-77 intercellular adhesion molecule 1 Homo sapiens 21-27 7864660-10 1994 These results indicate that the metals studied are able to induce an aggressive cellular effect, and that nickel, by its ICAM-1 induction, may play a major role in the keratinocyte activation state during allergic contact dermatitis. Nickel 106-112 intercellular adhesion molecule 1 Homo sapiens 121-127 1682230-3 1991 In nickel-sensitive individuals, after application of a nickel patch, increased expression of ICAM-1 on keratinocytes was observed as early as 3 h and reached a maximum at 48 h. The number of lymphocytes expressing LFA-1 in the dermis and epidermis was greatest at 48 h. The LFA-1 cells were observed to be in close proximity to keratinocytes expressing ICAM-1, thus supporting the hypothesis that T-lymphocytes attach to keratinocytes via LFA-1/ICAM-1 molecules. Nickel 3-9 intercellular adhesion molecule 1 Homo sapiens 94-100 1682230-3 1991 In nickel-sensitive individuals, after application of a nickel patch, increased expression of ICAM-1 on keratinocytes was observed as early as 3 h and reached a maximum at 48 h. The number of lymphocytes expressing LFA-1 in the dermis and epidermis was greatest at 48 h. The LFA-1 cells were observed to be in close proximity to keratinocytes expressing ICAM-1, thus supporting the hypothesis that T-lymphocytes attach to keratinocytes via LFA-1/ICAM-1 molecules. Nickel 3-9 intercellular adhesion molecule 1 Homo sapiens 354-360 9536222-3 1998 In proliferative HaCaT cells, following a 24 h exposure, nickel compounds, para-phenylenediamine (pPD) and 1-chloro-2,4-dinitrobenzene produced a concentration-dependent up-regulation of ICAM-1 expression without reducing cell viability, while K2Cr2O7 led to ICAM-1 up-regulation at cytotoxic concentrations, and CrCl3 was without effect. Nickel 57-63 intercellular adhesion molecule 1 Homo sapiens 187-193 9536222-3 1998 In proliferative HaCaT cells, following a 24 h exposure, nickel compounds, para-phenylenediamine (pPD) and 1-chloro-2,4-dinitrobenzene produced a concentration-dependent up-regulation of ICAM-1 expression without reducing cell viability, while K2Cr2O7 led to ICAM-1 up-regulation at cytotoxic concentrations, and CrCl3 was without effect. Nickel 57-63 intercellular adhesion molecule 1 Homo sapiens 259-265 7747530-5 1995 Using FACS analysis, we showed that the combination of zinc with nickel or the addition of ZnSO4 24 h before IFN-gamma or NiSO4 treatments reduced ICAM-1 expression on the keratinocyte surface (p < 0.01). Nickel 65-71 intercellular adhesion molecule 1 Homo sapiens 147-153 1682230-3 1991 In nickel-sensitive individuals, after application of a nickel patch, increased expression of ICAM-1 on keratinocytes was observed as early as 3 h and reached a maximum at 48 h. The number of lymphocytes expressing LFA-1 in the dermis and epidermis was greatest at 48 h. The LFA-1 cells were observed to be in close proximity to keratinocytes expressing ICAM-1, thus supporting the hypothesis that T-lymphocytes attach to keratinocytes via LFA-1/ICAM-1 molecules. Nickel 3-9 intercellular adhesion molecule 1 Homo sapiens 354-360 1682230-3 1991 In nickel-sensitive individuals, after application of a nickel patch, increased expression of ICAM-1 on keratinocytes was observed as early as 3 h and reached a maximum at 48 h. The number of lymphocytes expressing LFA-1 in the dermis and epidermis was greatest at 48 h. The LFA-1 cells were observed to be in close proximity to keratinocytes expressing ICAM-1, thus supporting the hypothesis that T-lymphocytes attach to keratinocytes via LFA-1/ICAM-1 molecules. Nickel 56-62 intercellular adhesion molecule 1 Homo sapiens 94-100 24080332-3 2013 Following screening of fifteen metals, zinc and nickel were identified with a marked proinflammatory effect, as determined by ICAM-1 and IL-8 induction, on human umbilical vein endothelial cells (HUVECs). Nickel 48-54 intercellular adhesion molecule 1 Homo sapiens 126-132 24080332-5 2013 Blockage of TLR-4 signaling by CLI-095, a TLR-4 inhibitor, completely inhibited the nickel-induced ICAM-1 and IL-8 expression and NFkappaB activation. Nickel 84-90 intercellular adhesion molecule 1 Homo sapiens 99-105 15715515-1 2005 OBJECTIVE: Nickel and cobalt ions activate ICAM1 expression on endothelial cells and keratinocytes. Nickel 11-17 intercellular adhesion molecule 1 Homo sapiens 43-48 15715515-12 2005 Supplemental experiments using nickel ions alone confirmed that ICAM1 was inducible on the endothelial cells by Ni(II) concentrations above 100 microM. Nickel 31-37 intercellular adhesion molecule 1 Homo sapiens 64-69