Polyclonal antibody directed against human RANTES ameliorates disease in the Lewis rat adjuvant-induced arthritis model.

Barnes, Debra A.; Tse, Joyce C.; Kaufhold, M; Owen, Markus R.; Hesselgesser, Joseph; Strieter, R. M.; Horuk, Richard; Perez, H D

doi:10.1172/jci2172

Cited by 169 publications

(131 citation statements)

References 41 publications

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“…After all, it probably augments a pre-existing response that, to begin with, is not sufficient to entirely suppress the development of an autoimmune condition. Interestingly, targeting the function of a single proinflammatory mediator suppresses a disease regulated by various cytokines and chemokines (13,(43)(44)(45)(46)(47)(48)(49)(50). These results are very surprising since different chemokines bind and activate common chemokine receptors.…”

Section: Discussionmentioning

confidence: 99%

“…Thereafter, Gong et al (12) used an antagonist of monocyte chemoattractant protein 1 (MCP-1) to inhibit arthritis in the MRL/lpr mouse model. Later, Barnes et al (13) used antihuman RANTES to ameliorate AA in the Lewis rat. Last, in a very recent study Fife et al (14) used anti-IFN-␥-inducible protein 10 (IP-10) Ab to inhibit experimental autoimmune encephalomyelitis.…”

Section: Targeting the Function Of Ifn-␥-inducible Protein 10mentioning

confidence: 99%

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Targeting the Function of IFN-γ-Inducible Protein 10 Suppresses Ongoing Adjuvant Arthritis

Salomon¹,

Netzer²,

Wildbaum³

et al. 2002

The Journal of Immunology

122

115

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IFN-γ-inducible protein 10 (IP-10) is a CXC chemokine that is thought to manifest a proinflammatory role because it stimulates the directional migration of activated T cells, particularly Th1 cells. It is an open question whether this chemokine is also directly involved in T cell polarization. We show here that during the course of adjuvant-induced arthritis the immune system mounts a notable Ab titer against self-IP-10. Upon the administration of naked DNA encoding IP-10, this titer rapidly accelerates to provide protective immunity. Self-specific Ab to IP-10 developed in protected animals, as well as neutralizing Ab to IP-10 that we have generated in rabbits, could inhibit leukocyte migration, alter the in vivo and in vitro Th1/Th2 balance toward low IFN-γ, low TNF-α, high IL-4-producing T cells, and adoptively transfer disease suppression. This not only demonstrates the pivotal role of this chemokine in T cell polarization during experimentally induced arthritis but also suggests a practical way to interfere in the regulation of disease to provide protective immunity. From the basic science perspective, this study challenges the paradigm of in vivo redundancy. After all, we did not neutralize the activity of other chemokines that bind CXCR3 (i.e., macrophage-induced gene and IFN-inducible T cell α chemoattractant) and yet significantly blocked not only adjuvant-induced arthritis but also the in vivo competence to mount delayed-type hypersensitivity.

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Section: Discussionmentioning

confidence: 99%

Section: Targeting the Function Of Ifn-␥-inducible Protein 10mentioning

confidence: 99%

Targeting the Function of IFN-γ-Inducible Protein 10 Suppresses Ongoing Adjuvant Arthritis

Salomon¹,

Netzer²,

Wildbaum³

et al. 2002

The Journal of Immunology

122

115

View full text Add to dashboard Cite

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“…An additional factor which may enhance the specificity of CC chemokines for target cells is the cellular distribution of the receptors. Moreover, most CCRs bind to multiple CC chemokines with different affinities (3,(7)(8)(9).…”

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confidence: 99%

“…Administration of neutralizing antibodies against the CC chemokines MCP-1, MIP-1␣, and RANTES delayed the onset of arthritis and reduced the severity of the disease in rodents (9,(19)(20)(21). Leukocytes are believed to be recruited from the circulation to the synovial tissue and to migrate into the joint space (22).…”

mentioning

confidence: 99%

Chemokine receptor expression and in vivo signaling pathways in the joints of rats with adjuvant‐induced arthritis

Shahrara¹,

Amin²,

Woods³

et al. 2003

Arthritis & Rheumatism

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Objective. This study was undertaken to characterize the role of CC chemokines and their receptors in rat adjuvant-induced arthritis (AIA), a model for rheumatoid arthritis (RA). Furthermore, we investigated the signaling pathways associated with CC receptors as well as the cell type distribution of the receptors.Methods. Using TaqMan real-time reverse transcription-polymerase chain reaction, Western blot analysis, and immunohistochemistry, we defined chemokine and chemokine receptor messenger RNA (mRNA) expression, CC chemokine receptor (CCR) protein activation during the disease course, CCRassociated signaling pathways, and immunopositive CCR5, phosphorylated signal transducer and activator of transcription 1 (p-STAT-1), and p-STAT-3 cells in rat AIA versus control joints.Results. We showed significant up-regulation of CCR1, CCR2, CCR5, and macrophage inflammatory protein 1␤/CCL4 mRNA in AIA on post-adjuvant injection day 18, coincident with peak inflammation. Additionally, increases in tyrosine phosphorylation of CCR1 (days 14, 18, 21, and 24), CCR2 (days 14 and 18), and CCR5 (days 14, 18, and 21) were detected in AIA rats compared with control (nonarthritic) rats. JAK-1, STAT-1, and STAT-3 were associated with CCR1 and were highly tyrosine phosphorylated on days 14 and 18. Rheumatoid arthritis (RA) is an inflammatory disorder characterized by infiltration of monocytes, T cells, and polymorphonuclear cells into the synovial joints. The CC chemokines monocyte chemoattractant protein 1 (MCP-1)/CCL2, macrophage inflammatory protein 1␣ (MIP-1␣)/CCL3, MIP-1␤/CCL4, and

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“…The notion that RANTES plays a role in the pathogenesis of chronic arthritis is strengthened by the results of studies of animal models of arthritis (2,3) and adults with RA (4,5). The results of the aforementioned studies indicate that RANTES is an attractive gene candidate for the genetic dissection of JRA.…”

mentioning

confidence: 99%

Association of RANTES promoter polymorphism with juvenile rheumatoid arthritis

Yao¹,

Tsai²,

Huang³

2009

Arthritis & Rheumatism

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Objective. We recently reported that RANTES was a key molecule in the pathogenesis of juvenile rheumatoid arthritis (JRA) in a longitudinal cohort. This study was undertaken to investigate genetic associations between the RANTES ؊28 C/G and ؊403 G/A polymorphisms and JRA in a well-documented cohort of patients who were followed up prospectively.Methods. Patients with JRA (n ‫؍‬ 107) and healthy children (n ‫؍‬ 139) were genotyped through use of a polymerase chain reaction-based assay. Association of the RANTES promoter polymorphisms with results of laboratory tests, clinical variables, outcome after clinical remission, and response to intraarticular triamcinolone injection was evaluated in patients who were followed up for >1 year.Results. JRA patients had a significantly higher frequency of the RANTES ؊28 G/G genotype, as compared with ethnically matched healthy controls. The RANTES ؊28 C/G polymorphism was associated with the duration of clinical remission, with patients carrying the RANTES -28G allele experiencing only 49% of the duration of remission experienced by patients who were RANTES ؊28 C/C homozygous. The RANTES ؊28 C/G polymorphism was associated with the duration of clinical response to intraarticular triamcinolone injection, with patients carrying the RANTES ؊28G allele showing shorter duration of clinical response. No significant association between the RANTES ؊403 G/A polymorphism and JRA was found in this Chinese population.Conclusion. Our findings indicate that the RANTES ؊28 C/G polymorphism represents a genetic risk factor for JRA. It is noteworthy that this RANTES promoter polymorphism was also associated with an early relapse of disease after clinical remission and a shorter duration of clinical response to intraarticular administration of corticosteroids.Juvenile rheumatoid arthritis (JRA) is the most common rheumatic disease in children. We have recently reported that RANTES, a CC chemokine also known as CCL5, is a key molecule in JRA pathogenesis (1). Increased levels of RANTES have been found in both sera and synovial fluid from children with JRA, and serum RANTES levels represent a more highly sensitive marker of disease activity than do conventional markers of inflammation (1). We also previously demonstrated an inverse correlation between serum RANTES levels in remission and the duration of clinical remission, with low RANTES levels being associated with prolonged clinical remission and high levels with shorter clinical remission (1). Furthermore, we identified RANTES as a chemoattractant for mononuclear leukocytes to inflamed joints in JRA (1).The notion that RANTES plays a role in the pathogenesis of chronic arthritis is strengthened by the results of studies of animal models of arthritis (2,3) and adults with RA (4,5). The results of the aforementioned studies indicate that RANTES is an attractive gene candidate for the genetic dissection of JRA. It has been demonstrated that 2 RANTES promoter polymorphisms (Ϫ28 C/G and Ϫ403 G/A) elevate promoter activity and increase RANTES expr...

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Polyclonal antibody directed against human RANTES ameliorates disease in the Lewis rat adjuvant-induced arthritis model.

Cited by 169 publications

References 41 publications

Targeting the Function of IFN-γ-Inducible Protein 10 Suppresses Ongoing Adjuvant Arthritis

Targeting the Function of IFN-γ-Inducible Protein 10 Suppresses Ongoing Adjuvant Arthritis

Chemokine receptor expression and in vivo signaling pathways in the joints of rats with adjuvant‐induced arthritis

Association of RANTES promoter polymorphism with juvenile rheumatoid arthritis

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