VLA family in rheumatoid arthritis: evidence for<i>in vivo</i>regulated adhesion of synovial fluid T cells to fibronectin through VLA-5 integrin

García‐Vicuña, Rosario; Humbría, Alicia; Postigo, Antonio; López-Elzaurdia, C.; Landázuri, Manuel O.; Sánchez‐Madrid, Francisco; Laffón, A

doi:10.1111/j.1365-2249.1992.tb06468.x

Cited by 22 publications

(1 citation statement)

References 45 publications

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“…Defining the phenotype of the migrating monocytes is of interest because we have shown in this study that monocytes infected in vitro did not have an increased expression of the common adhesion molecules (ICAM-1, VCAM-1, or PE-CAM-1). The implication of other adhesion molecules such as those from the VLA family remains to be determined, as well as the pattern of chemokine receptors they express, because these molecules may direct the infected monocytes to specific tissues as demonstrated for rheumatoid arthritis (52).…”

Section: Discussionmentioning

confidence: 99%

Active Infection of Human Blood Monocytes by Chikungunya Virus Triggers an Innate Immune Response

Her

Malleret

Chan

et al. 2010

The Journal of Immunology

250

254

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Chikungunya virus (CHIKV) is an alphavirus that causes chronic and incapacitating arthralgia in humans. To date, interactions between the immune system and the different stages of the virus life cycle remain poorly defined. We demonstrated for the first time that CHIKV Ags could be detected in vivo in the monocytes of acutely infected patients. Using in vitro experimental systems, whole blood and purified monocytes, we confirmed that monocytes could be infected and virus growth could be sustained. CHIKV interactions with monocytes, and with other blood leukocytes, induced a robust and rapid innate immune response with the production of specific chemokines and cytokines. In particular, high levels of IFN-α were produced rapidly after CHIKV incubation with monocytes. The identification of monocytes during the early phase of CHIKV infection in vivo is significant as infected monocyte/macrophage cells have been detected in the synovial tissues of chronically CHIKV-infected patients, and these cells may behave as the vehicles for virus dissemination. This may explain the persistence of joint symptoms despite the short duration of viremia. Our results provide a better understanding on the basic mechanisms of infection and early antiviral immune responses and will help in the development of future effective control strategies.

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Section: Discussionmentioning

confidence: 99%

Active Infection of Human Blood Monocytes by Chikungunya Virus Triggers an Innate Immune Response

Her

Malleret

Chan

et al. 2010

The Journal of Immunology

250

254

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Differential Distribution of Intercellular Adhesion Molecules (ICAM–1, ICAM–2, and ICAM–3) and THE MS–1 Antigen in Normal and Diseased Human Synovia

Szekanecz

Haines

Lin

et al. 1994

Arthritis & Rheumatism

129

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Objective. Cellular adhesion and differentiation molecules (CAMs) may play a role in the recruitment and retention of inflammatory cells into rheumatoid arthritis synovial tissue (RA ST). In order to determine if certain CAMs are up‐regulated in RA ST compared with normal ST, we studied the distribution of intercellular adhesion molecules (ICAMs) 1, 2, and 3 in ST. We also studied the MS‐1 antigen since it is preferentially expressed on discontinuous endothelia, such as those found in RA ST; MS‐1 is also expressed differentially upon cytokine activation of cells in vitro or in pathologic conditions in situ. Thus, we postulated a possible similarity between MS‐1 and ICAM‐1 expression in inflamed ST. Methods. Immunohistochemical analysis was used to determine the distribution of ICAMs and MS‐1 in ST from 10 patients with RA, 10 with osteoarthritis (OA), and 4 normal individuals. Results. ICAM‐1 expression was found on significantly more RA ST endothelial cells compared with normal cells, as well as on RA ST macrophages and lining cells. ICAM‐2, also found on endothelial cells, showed no differential staining pattern. ICAM‐3 was present on RA ST macrophages and lining cells as well as on some RA and OA endothelial cells. The MS‐1 antigen was present on most RA and OA ST endothelia, lining cells, and macrophages. ICAM‐1 expression and MS‐1 expression in the lining layer were positively correlated in both RA and OA. Conclusion. ICAM‐1, while found mainly on endothelial cells, is up‐regulated on RA ST macrophages and lining cells, suggesting a role for these cells in the infiltration and tissue damage seen in the RA ST. ICAM‐3, which is present mainly on normal resting leukocytes but not on normal endothelium, is expressed by some diseased ST leukocytes and endothelial cells. MS‐1 is also found on the RA ST specialized, fenestrated endothelium, on macrophages, and in the lining layer. These results suggest that the differential expression of ICAMs and MS‐1 in RA ST compared with normal ST might play a special role in the pathogenesis of RA.

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Signal transduction through chondrocyte integrin receptors induces matrix metalloproteinase synthesis and synergizes with interleukin‐1

Arner

Tortorella

1995

Arthritis & Rheumatism

112

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Objective. To study the role of signal transduction via integrin receptors in the production of metalloproteinase by rabbit articular chondrocytes.Methods. Confluent, primary rabbit articular chondrocytes (RAC) were incubated for 72 hours in the presence of interleukin-1 (IL-1), Arg-Gly-Asp (RGD) peptide, or a combination of IL-1 and RGD peptide. Media were analyzed for stromelysin enzymatic activity using a 3H-labeled transferrin substrate, and for stromelysin and collagenase protein by Western analysis. Gelatinase activity was analyzed by gelatin zymography. IL-1 receptor antagonist (IL-1Ra) protein was used to determine the involvement of IL-1 in mediating the effects of RGD peptide, and fluorescence-activated cell sorter analysis (FACS) was used to examine the effect of IL-1 on chondrocyte integrin subunit expression.Results. RGD peptides induced chondrocyte synthesis of stromelysin, collagenase, and 92-kd gelatinase B, and increased synthesis of the constitutively expressed 72-kd gelatinase A. Further studies focusing on stromelysin demonstrated that this up-regulation was concentration dependent and that RGD peptides synergized with IL-1 in inducing stromelysin synthesis. RGDinduced stromelysin production was inhibited by the IL-1Ra in a concentration-dependent manner, indicating that induction by RGD requires binding of IL-1 to its receptor. FACS analysis of RAC showed that IL-1 stimulation increased the expression of pl and (yv integrin subunits on the chondrocyte surface.

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VLA family in rheumatoid arthritis: evidence forin vivoregulated adhesion of synovial fluid T cells to fibronectin through VLA-5 integrin

Cited by 22 publications

References 45 publications

Active Infection of Human Blood Monocytes by Chikungunya Virus Triggers an Innate Immune Response

Active Infection of Human Blood Monocytes by Chikungunya Virus Triggers an Innate Immune Response

Differential Distribution of Intercellular Adhesion Molecules (ICAM–1, ICAM–2, and ICAM–3) and THE MS–1 Antigen in Normal and Diseased Human Synovia

Signal transduction through chondrocyte integrin receptors induces matrix metalloproteinase synthesis and synergizes with interleukin‐1

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