Inflammation, Immune Reactivity, and Angiogenesis in a Severe Combined Immunodeficiency Model of Rheumatoid Arthritis

Davis, Laurie S.; M, Sackler; Brezinschek, Ruth I.; Lightfoot, Ellis; Bailey, Jennifer L.; Oppenheimer‐Marks, Nancy; Lipsky, Peter E.

doi:10.1016/s0002-9440(10)64379-9

Cited by 34 publications

(30 citation statements)

References 35 publications

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“…In RA patient the immune system is rather activated than suppressed (Davis et al 2002). In this study, the incidence and density of D. folliculorum in patients with RA were not significantly different from these of controls.…”

Section: Discussioncontrasting

confidence: 55%

Demodex folliculorum in patients with rheumatoid arthritis

Çiftçi

Dündar

Çetınkaya

et al. 2007

Acta Parasitologica

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The objective of this study was to investigate the incidence and density of Demodex folliculorum in the patients with rheumatoid arthritis (RA). Forty-one patients with RA and twenty-seven age and sex matched healthy controls were enrolled in this study. Disease Activity Score (DAS 28) was used for the assessment of disease activity. Out of 41 patients, 33 were females and 8 males. The mean disease duration was 10.9 ± 8.2 years. The mean DAS 28 was 3.8 ± 1.2. No statistically significant differences in the incidence and density of Demodex mites were found between patients with RA and controls. Although immunosuppression is thought to be a risk factor for the D. folliculorum infestation no such correlations could be found in the 41 immunosuppressed patients with RA, therefore, further studies with larger groups are needed.

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Section: Discussioncontrasting

confidence: 55%

Demodex folliculorum in patients with rheumatoid arthritis

Çiftçi

Dündar

Çetınkaya

et al. 2007

Acta Parasitologica

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“…2, A and C; Table I). Appearances resembled those of CFAinduced CIA (30) and RA synovial tissue (33,34). Commensurate with clinical observations, joints of mice receiving unpulsed DCs exhibited no apparent local inflammatory reaction (Fig.…”

Section: Collagen-pulsed Dcs Induce Arthritis In Recipient Micesupporting

confidence: 65%

A Novel Dendritic Cell-Induced Model of Erosive Inflammatory Arthritis: Distinct Roles for Dendritic Cells in T Cell Activation and Induction of Local Inflammation

Leung

Conacher

Hunter

et al. 2002

The Journal of Immunology

101

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Transferring collagen-pulsed, bone marrow-derived dendritic cells (DCs) into congenic DBA/1 recipient mice produced arthritis in joints adjacent to the site of DC transfer and could be inhibited by treatment with TNF antagonists. Disease was Ag specific, as transfer of control, unpulsed DCs, or DCs pulsed with OVA did not produce arthritis. In contrast to other experimental arthritis models, DC-induced arthritis localized to the site of injection and did not spontaneously generalize to uninvolved joints, despite the demonstration of circulating collagen-reactive T cells. Similarly, transfer of T cells primed by collagen/DCs was not sufficient to produce arthritis in recipient mice. In collagen/DC-primed mice however, disease could be induced in uninvolved joints by local administration of noncollagen-pulsed DCs and this could be reduced through TNF inhibition. Similarly, injection of collagen/DC-primed mice with low-dose TNF also resulted in local induction of arthritis, as did administration of TNF to mice receiving T cells from collagen/DC but not OVA/DC-primed mice. Thus, we have demonstrated for the first time that administration of collagen-pulsed mature DCs is sufficient for the induction of arthritis. Furthermore, this disease process is mediated through both adaptive and innate effects of DCs; first, priming of autoreactive T cells and, second, induction of local inflammation via mediators such as TNF.

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“…This model has been used successfully by other groups to show that engrafted RA ST not only keeps many of the morphologic and pathologic characteristics of RA ST (62), but also can be used as an appropriate model of RA (63). We found that tail vein-injected cells migrate to engrafted RA ST and murine LNs in response to intragraft injections of human CXCL16.…”

Section: Discussionmentioning

confidence: 75%

CXCL16‐mediated cell recruitment to rheumatoid arthritis synovial tissue and murine lymph nodes is dependent upon the MAPK pathway

Ruth¹,

Haas²,

Park³

et al. 2006

Arthritis & Rheumatism

107

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Objective. Rheumatoid arthritis (RA) is characterized by profound mononuclear cell (MNC) recruitment into synovial tissue (ST), thought to be due in part to tumor necrosis factor ␣ (TNF␣), a therapeutic target for RA. Although chemokines may also be involved, the mechanisms remain unclear. We undertook this study to examine the participation of CXCL16, a novel chemokine, in recruitment of MNCs to RA ST in vivo and to determine the signal transduction pathways mediating this process. Conclusion. Taken together, these results point to a unique role for CXCL16 as a premier MNC recruiter in RA and suggest additional therapeutic possibilities, targeting CXCL16, its receptor, or its signaling pathways.

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Inflammation, Immune Reactivity, and Angiogenesis in a Severe Combined Immunodeficiency Model of Rheumatoid Arthritis

Cited by 34 publications

References 35 publications

Demodex folliculorum in patients with rheumatoid arthritis

Demodex folliculorum in patients with rheumatoid arthritis

A Novel Dendritic Cell-Induced Model of Erosive Inflammatory Arthritis: Distinct Roles for Dendritic Cells in T Cell Activation and Induction of Local Inflammation

CXCL16‐mediated cell recruitment to rheumatoid arthritis synovial tissue and murine lymph nodes is dependent upon the MAPK pathway

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