CD4+CD25+ Regulatory T Cells Protect against Injury in an Innate Murine Model of Chronic Kidney Disease

Mahajan, Deepika; Wang, Yiping; Qin, Xiahong; Wang, Ying; Zheng, Guoping; Wang, Yuan Min; Alexander, Stephen I.; Harris, David C.H.

doi:10.1681/asn.2005080842

Cited by 127 publications

(114 citation statements)

References 37 publications

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“…As Tregs have anti-inflammatory properties, their presence is protective to renal injury. [95][96][97] Tregs suppress production of MIP-1␣/CCL3 by macrophages, which in turn protects against macrophage-dependent, lymphocyte-independent injury. 95 Studies from CCR7 null mice demonstrate that CCR7 on Tregs is critical for homing of Tregs to lymphoid organs and guiding the Tregs to sites of antigen-specific activation.…”

Section: Role Of Chemokines In T Cell Infiltration During Kidney Injurymentioning

confidence: 99%

“…[95][96][97] Tregs suppress production of MIP-1␣/CCL3 by macrophages, which in turn protects against macrophage-dependent, lymphocyte-independent injury. 95 Studies from CCR7 null mice demonstrate that CCR7 on Tregs is critical for homing of Tregs to lymphoid organs and guiding the Tregs to sites of antigen-specific activation. 98 -100 Importantly, adoptive transfer of CCR7 ϩ Tregs, but not CCR7-Tregs, into CCR7 null mice restores Treg numbers in lymphoid organs and ameliorates disease.…”

Section: Role Of Chemokines In T Cell Infiltration During Kidney Injurymentioning

confidence: 99%

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Chemokines in Renal Injury

Chung

Lan

2011

Journal of the American Society of Nephrology

240

181

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Renal inflammation underlies many chronic kidney diseases and the infiltration of leukocytes mediates much of the nephritogenic inflammatory response. As several recent reviews have dealt with the basic biology, mouse models, and blockade studies of chemokines in renal diseases, [1][2][3][4][5][6][7][8][9][10][11] we focus here on recent developments in pathophysiology of that chemokine effect. CHEMOKINES AND CHEMOKINE RECEPTORSChemokines are a group of chemotactic cytokines (approximately 8 to 17 kD) with the ability to bind G-proteincoupled receptors and act as potent attractants for leukocytes in acute and chronic inflammation. There are four subfamilies of chemokines, including CCL, CXCL, CX3CL, and CL (Figure 1). 7,6 At present, 19 receptors are known ( Figure 1). 6,7 The large CC chemokine family has the first two cysteine residues adjacent to each other, whereas the CXC family has a single amino acid residue in between the first two cysteines. Fractalkine (CX3CL1) is the only member of the CX3C chemokine family where three amino acid residues separate the first two cysteines. Finally, two related chemokines absent the two cysteine residues that bind the XCR1 receptor belong to the XC family. As shown in Figure 1, many chemokines bind multiple receptors and most receptors bind multiple chemokines. However, CC chemokine receptors exclusively bind CC chemokines and CXC receptors bind only CXC chemokines.Chemokines and their corresponding receptors are expressed in different cell types (Figure 2). 7,12 Generally speaking, monocytes are mostly attracted by CCL chemokines acting through CCR1, CCR2, andCCR5receptors,whereasneutrophilsare the target of CXCL chemokines through REGULATION OF CHEMOKINE EXPRESSIONOn the basis of their regulation and production, chemokines can be classified broadly as homeostatic/lymphoid or inflammatory chemokines. The former is responsible for leukocyte homing and ABSTRACTThe main function of chemokines is to guide inflammatory cells in their migration to sites of inflammation. During the last 2 decades, an expanding number of chemokines and their receptors have driven broad inquiry into how inflammatory cells are recruited in a variety of diseases. Although this review focuses on chemokines and their receptors in renal injury, proinflammatory IL-17, TGF␤, and TWEAK signaling pathways also play a critical role in their expression. Recent studies in transgenic mice as well as blockade of chemokine signaling by neutralizing ligands or receptor antagonists now allow direct interrogation of chemokine action. The emerging role of regulatory T cells and Th17 cells during renal injury also forges tight relationships between chemokines and T cell infiltration in the development of kidney disease. As chemokine receptor blockade inches toward clinical use, the field remains an attractive area with potential for unexpected opportunity in the future.

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Section: Role Of Chemokines In T Cell Infiltration During Kidney Injurymentioning

confidence: 99%

Section: Role Of Chemokines In T Cell Infiltration During Kidney Injurymentioning

confidence: 99%

Chemokines in Renal Injury

Chung

Lan

2011

Journal of the American Society of Nephrology

240

181

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“…103,104 The ability of DC to process and present antigen can also be suppressed after contact with Treg, 105,106 raising the possibility that resident rDC themselves are targets for trafficking Treg. Notably, Treg ameliorate both the acute and chronic phases of renal disease in disparate models of immune-mediated renal injury, [107][108][109] although rDC-Treg interactions have not been studied in these experiments. This possible interaction is an exciting area of future inquiry, as is the potential to manipulate the reciprocal relationship between rDC and Treg to suppress immune responses that may be coordinated by rDC.…”

Section: Adaptive Immunitymentioning

confidence: 99%

Dendritic Cells in the Kidney

Nelson¹

2007

Journal of the American Society of Nephrology

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“…In addition to their expression of CD4 and CD25, these cells are anergic to proliferative responses in vitro and do not express key cytokines, including IL-2 or IFN-in response to stimulation [8,9]. Functionally, they are characterized by the capacity to suppress proliferation of effector T cells in vitro in a process requiring activation and cell contact but not IL-4, IL-10, or transforming growth factor-(TGF-) [10].…”

Section: Introductionmentioning

confidence: 99%