Recruitment of CXCR3+ and CCR5+ T Cells and Production of Interferon-γ-Inducible Chemokines in Rejecting Human Arteries

Burns, William R.; Wang, Yinong; Tang, Paul C.; Ranjbaran, Hooman; Iakimov, Alexander O.; Kim, Jinah; Cuffy, Madison C.; Bai, Yalai; Pober, Jordan S.; Tellides, George

doi:10.1111/j.1600-6143.2005.00892.x

Cited by 69 publications

(55 citation statements)

References 37 publications

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“…[32][33][34] We have reached similar conclusions with our investigations in a chimeric human-animal model in which human coronary arteries are interposed into the aortae of severe combined immunodeficient (SCID) mouse hosts that are subsequently reconstituted with allogeneic human peripheral blood mononuclear cells. 35 In this model, intimal expansion and outward vascular remodeling in response to allogeneic human T cells is dependent on IFN-␥, 36 neutralization of IFN-␥ can prevent T cell-mediated EC and VSMC dysfunction, 37 IFN-␥-inducible chemokine production by vascular cells is associated with the recruitment of T H 1 cells, 38 and immunosuppressive agents that prevent intimal expansion also reduce IFN-␥ synthesis and responses. 39 Finally, administration of human IFN-␥ alone, in the absence of leukocytes, is sufficient to induce arteriosclerosis in the transplanted human arteries.…”

Section: Evidence For a Pathogenetic Role Of Ifn-␥ In Gamentioning

confidence: 99%

“…A pathway of selective recruitment, judged by selective CXCR3-binding chemokine expression, does appear to operate in human GA, [23][24][25][26][27] as well as in our human artery GA model. 38 These studies have demonstrated that CXCR3 and CCR5 ligands are synthesized in both the parenchymal and vascular compartments of human cardiac allografts. However, a direct comparison of the production of IFN-␥-inducible chemokines by microvascular ECs (parenchymal versus large artery adventitial microvessels) and large artery luminal ECs has not been performed; such a comparison may be informative about the mechanisms responsible for selective accumulation of T H 1 cells in the vascular compartment during the pathogenesis of GA. T-cell recruitment may be species specific because many EC molecules that are involved in interactions with T cells show species differences.…”

Section: T H 1 Effector Cells and Cd8mentioning

confidence: 99%

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Interferon-γ Axis in Graft Arteriosclerosis

Tellides

Pober

2007

Circulation Research

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107

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Abstract-Cardiac transplantation is the most effective treatment for advanced heart failure. Despite improvements in immunosuppression therapy that prevent acute rejection, cardiac allografts fail at rates of 3% to 5% per posttransplant year. The hallmark morphological lesion of chronically failing cardiac allografts, also seen in chronic renal and liver graft failure, is luminal stenosis of blood vessels, especially of conduit arteries. Late graft failure results from widespread secondary ischemic injury to the graft parenchyma rather than direct immune-mediated damage. Although this process affects the entire graft vasculature, graft arteriosclerosis is a suitable term to describe the problem because it applies to different types of failing organs and because it emphasizes the central feature, namely an accelerated form of arterial injury and remodeling. The precise pathogenesis of graft arteriosclerosis is unknown. In this review, we make the case that the signature T-helper type 1 cytokine, interferon (IFN)-␥, is a key effector in graft arteriosclerosis, which, together with the IFN-␥-inducing cytokine interleukin-12 and IFN-␥-inducible chemokines such as CXCR3 ligands, constitute a positive feedback loop for T-cell activation, differentiation, and recruitment that we refer to as the IFN-␥ axis. We evaluate the evidence to support this hypothesis in clinical observational and experimental animal studies. Additionally, we examine the regulation of IFN-␥ production within the artery wall, the effects of IFN-␥ on vessel wall cells, and the outcome of therapeutic agents on IFN-␥ production and signaling. These observations lead us to suggest that new therapies for graft arteriosclerosis should be optimized which focus on reducing IFN-␥ synthesis or actions. (Circ Res. 2007;100:622-632.)

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Section: Evidence For a Pathogenetic Role Of Ifn-␥ In Gamentioning

confidence: 99%

Section: T H 1 Effector Cells and Cd8mentioning

confidence: 99%

Interferon-γ Axis in Graft Arteriosclerosis

Tellides

Pober

2007

Circulation Research

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107

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“…IP-10 is one of chemokines toward CXCR3, has a chemotaxis for monocytes and Th1 cells, and is produced by fibroblasts and vascular endothelial cells, [26][27][28] while CXCR3 and CCR5 are specific chemokine receptors for Th1 cells. 29,30 The expression of both Th1 chemokines and chemokine receptors in the oral lesions indicates that Th1 cells possibly migrate there from the circulation.…”

Section: Cytokines Chemokines and Chemokine Receptors Involvement Inmentioning

confidence: 99%

Possible involvement of cytokines, chemokines and chemokine receptors in the initiation and progression of chronic GVHD

Nakamura

Toyoshima

Moriyama

et al. 2012

Bone Marrow Transplant

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Chronic GVHD (cGVHD) after allogeneic hematopoietic SCT (HSCT) is characterized by an infiltration of T cells into target organs including the oral mucosa and salivary glands. This study was designed to clarify the molecular mechanism of the local accumulation of pathogenic T cells in cGVHD. The expression of cytokines, chemokines and chemokine receptors in the buccal mucosa (BM), labial salivary glands (LSG) and PBMC from 16 patients with cGVHD after allogeneic HSCT was examined. The mRNA expression of T helper 1 (Th1) and Th2 cytokines, and several chemokines and chemokine receptors was significantly increased in the BM and LSG from cGVHD patients, in comparison with both those in the BM and LSG from controls, respectively, and also with those in the PBMC from cGVHD patients. Furthermore, the mRNA expression of Th2 cytokines, macrophage-derived chemokine and CC chemokine receptor 4 was closely associated with a strong T-cell infiltration in the BM and LSG from cGVHD patients. These results suggest that cGVHD might be initiated and/or maintained by Th1/Th0 cells and thereafter progresses in association with Th2 cell accumulation via the interaction of particular chemokine and chemokine receptors.

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“…Vários estudos observaram que a expressão dos receptores CXCR3 e CCR5 está aumentada na inflamação com fenótipo 1, como ocorre na DPOC 19,53,66 69 . Essas células expressavam CXCR3 e CCR5.…”

Section: Quimiocinas Do Receptor Cxcr3unclassified

Células inflamatórias e seus mediadores na patogênese da DPOC

Costa

Rufino

Silva

2009

Rev. Assoc. Med. Bras.

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Artigo de revisão ResumoA doença pulmonar obstrutiva crônica (DPOC) é causada por processo inflamatório crônico que limita o fluxo aéreo, sendo sua principal causa o tabagismo. Conforme dados da Organização Mundial de Saúde (OMS), a DPOC será a quarta causa de mortalidade em 2020, atrás apenas das doenças vasculares, cardíacas e cerebral, além das neoplasias. Apesar do enorme crescimento da prevalência e da mortalidade da DPOC, não existe nenhuma terapêutica que consiga controlar a evolução da doença estabelecida. O processo inflamatório crônico causado pelos gases da fumaça de tabaco desencadeia alterações estruturais que predominam nas pequenas vias aéreas (menores que 2 mm). Essa agressão provoca um processo inflamatório que conta com a participação não apenas de macrófagos, linfócitos e neutrófilos, mas células estruturais como epiteliais, musculares e fibroblastos. Atualmente, a interação entre macrófagos e linfócitos, especialmente CD8+, tem sido implicada na patogênese da DPOC. Quimiocinas como CXCL9/MIG, CXCL10/IP-10, CXCL11/I-TAC e CCL5/RANTES têm sido descritas como possíveis responsáveis pelo recrutamento de linfócitos T e monócitos sanguíneos, facilitando o aumento de macrófagos alveolares e linfócitos T CD8+ no parênquima dos pacientes com DPOC. Conhecer melhor como ocorre o tráfego de células mononuclerares em direção ao pulmão é fundamental não só para um maior entendimento da patogênese da DPOC, mas para o desenvolvimento de terapêuticas adequadas. Com base nessas evidências tem sido proposto o estudo de moléculas capazes de bloquear de forma específica o recrutamento de células inflamatórias para o pulmão por meio de ação direta nos seus receptores.Unitermos: DPOC. Inflamação. Quimiocinas.células inflamatórias e seus mediadores na patogênese da dpoc

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Recruitment of CXCR3+ and CCR5+ T Cells and Production of Interferon-γ-Inducible Chemokines in Rejecting Human Arteries

Abstract: 1 These authors contributed equally to this work.

Cited by 69 publications

References 37 publications

Interferon-γ Axis in Graft Arteriosclerosis

Interferon-γ Axis in Graft Arteriosclerosis

Possible involvement of cytokines, chemokines and chemokine receptors in the initiation and progression of chronic GVHD

Células inflamatórias e seus mediadores na patogênese da DPOC

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