An Analysis of Monocyte/Macrophage Subsets and Granulocyte-Macrophage Colony-Stimulating Factor Expression in Renal Allograft Biopsies

Kajiwara, Ichiro; Kawamura, Ken; Takebayashi, S

doi:10.1159/000189137

Cited by 17 publications

(1 citation statement)

References 19 publications

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“…These studies collectively demonstrate that multiple chemokines are involved in the recruitment of macrophages into allografts during AR and blocking chemokine-induced signaling pathways may be a promising therapeutic strategy. Other studies have shown that local macrophages proliferate in AR [55,56,61], suggesting another mechanism for increasing the number of macrophages in allografts undergoing AR.…”

Section: Macrophages In Acute Allograft Rejectionmentioning

confidence: 99%

Macrophages in solid organ transplantation

et al. 2014

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Macrophages are highly plastic hematopoietic cells with diversified functions related to their anatomic location and differentiation states. A number of recent studies have examined the role of macrophages in solid organ transplantation. These studies show that macrophages can induce allograft injury but, conversely, can also promote tissue repair in ischemia-reperfusion injury and acute rejection. Therapeutic strategies that target macrophages to improve outcomes in solid organ transplant recipients are being examined in preclinical and clinical models. In this review, we discuss the role of macrophages in different types of injury and rejection, with a focus on macrophage-mediated tissue injury, specifically vascular injury, repair and remodeling. We also discuss emerging macrophage-centered therapeutic opportunities in solid organ transplantation.

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Section: Macrophages In Acute Allograft Rejectionmentioning

confidence: 99%

Macrophages in solid organ transplantation

et al. 2014

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Expression of growth arrest-specific gene�6 and its receptors in dysfunctional human renal allografts

Yin

Hambly

Bao

et al. 2003

Transplant International

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Growth arrest-specific gene 6 (Gas6) and its receptors Rse, Axl and Mer have recently been found to be involved in a rat model of chronic allograft nephropathy (CAN). Thus, in this study we investigated the function of Gas6 and its receptors in human renal allograft dysfunction. Expression of Gas6 and its receptors was detected by immunohistochemical staining. Gas6 and its receptors were widely expressed in glomeruli, tubules and vessels of renal allografts. Gas6 expression was detected in normal-functioning allografts and was increased in acute rejection ( P<0.05), acute tubular necrosis ( P<0.05) and CAN ( P<0.01). Gas6 receptors were not upregulated in any of the allograft groups, except for the Axl receptor, which increased only in acute tubular necrosis ( P<0.01). Gas6 expression was also found to correspond with the expression of alpha-smooth muscle actin, a general marker of CAN ( r(2)=0.21, P<0.01). These findings suggest that Gas6, acting as a growth factor, is increased in the process of kidney allograft dysfunction and in CAN.

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Humoral rejection of human organ transplants

Michaels

Fishbein

Colvin

2003

Springer Seminars in Immunopathology

139

117

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Although T-cell mediated rejection has remained the most common form of acute rejection, humoral rejection now accounts for a substantial fraction in patients with kidney or heart allografts, and probably causes the majority of acute graft losses. The frequency, variously estimated at 20-30%, is attributed to improved methods of detection, including staining for C4d in tissues, which is more sensitive and specific than histological features. Detection of circulating anti-donor reactive antibody (usually to donor HLA antigens) confirms the diagnosis. The clinico-pathological entity of acute humoral rejection is well accepted in kidney and increasingly in heart transplantation. Recent evidence points to a new category of chronic humoral rejection, which accounts for about 60% of chronic rejection of kidneys. Importantly, the hallmark of humoral rejection, C4d, can be detected in the grafts before development of histological evidence of chronic rejection. Humoral rejection is generally not responsive to the usual anti-T cell immunosuppressive agents, but small, non-controlled trials suggest humoral rejection can be reversed with plasmapheresis, intravenous immunoglobulin, anti-CD20 and other treatments, all of which deserve formal clinical evaluation. Prophylaxis for chronic rejection is expected to require donor-specific serological monitoring and protocol biopsies.

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An Analysis of Monocyte/Macrophage Subsets and Granulocyte-Macrophage Colony-Stimulating Factor Expression in Renal Allograft Biopsies

Cited by 17 publications

References 19 publications

Macrophages in solid organ transplantation

Macrophages in solid organ transplantation

Expression of growth arrest-specific gene�6 and its receptors in dysfunctional human renal allografts

Humoral rejection of human organ transplants

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