Chemokine Signaling Regulates Apoptosis as well as Immune Cell Traffic in Host Defense

Grayson, Mitchell H.; Holtzman, Michael J.

doi:10.4161/cc.5.4.2427

Cited by 9 publications

(6 citation statements)

References 20 publications

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“…Chemokines that have exhibited anti-apoptotic function include CCL25 [23, 33, 34], CXCL12 [17], CCL21 and CCL19 [3, 26, 32], CXCL13[3], and CCL5 [10]. In contrast, chemokines that have exhibited proapoptotic function include CXCL12 [5], CXCL9 [32], and CXCL10 [28, 32].…”

Section: Discussionmentioning

confidence: 99%

Association between decreased CXCL12 and CCL25 expression and increased apoptosis in lymphoid tissues of cynomolgus macaques during SIV infection

Qin

Sui

Murphey‐Corb

et al. 2008

J of Medical Primatology

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Background Chemokines likely play multiple roles in HIV-1 and SIV pathogenesis. To examine potential associations between chemokine expression levels and apoptosis of cells in lymphoid tissues during SIV infection, we measured chemokine and cytokine mRNA levels in multiple lymphoid tissues compartments from uninfected and SIV-infected cynomolgus macaques (Macaca fascicularis). Methods Real-time RT-PCR was used to measure host mRNA levels in macaque lymphoid tissues. Proliferating or apoptotic cells were identified in lymphoid tissues by immunohistochemistry. Results We found that CXCL12 and CCL25 mRNAs in SIV-infected lymphoid tissues were decreased and their levels were negatively correlated with the numbers of proliferating and apoptotic cells. In vitro analyses revealed that CXCL12 and CCL25 were capable of reducing apoptosis induced by SIV infection. Conclusions These findings suggest that increased apoptosis in lymphoid tissues due to reduced levels of anti-apoptotic chemokines might be a mechanism that contributes to loss of immune function following pathogenic SIV infection.

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Section: Discussionmentioning

confidence: 99%

Association between decreased CXCL12 and CCL25 expression and increased apoptosis in lymphoid tissues of cynomolgus macaques during SIV infection

Qin

Sui

Murphey‐Corb

et al. 2008

J of Medical Primatology

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“…Indeed, CCL5 has been shown to mediate apoptosis in T cells and virus-infected macrophages (27,28); XCL1 costimulates the apoptosis of human CD4 ϩ T cells (29), and CXCL12 has been implicated both in survival and apoptosis of T cells (30). Conversely, CXCL8 inhibits neutrophil apoptosis (31) and induces B cell chronic lymphocytic leukemia cell accumulation (32).…”

Section: Discussionmentioning

confidence: 99%

CCL2 Inhibits the Apoptosis Program Induced by Growth Factor Deprivation, Rescuing Functional T Cells

Díaz-Guerra

Vernal

Prete

et al. 2007

The Journal of Immunology

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The precise mechanisms involved in the switch between the clonal expansion and contraction phases of a CD8+ T cell response remain to be fully elucidated. One of the mechanisms implicated in the contraction phase is cytokine deprivation, which triggers apoptosis in these cells. CCR2 chemokine receptor is up-regulated following IL-2 deprivation, and its ligand CCL2 plays an essential role preventing apoptosis induced by IL-2 withdrawal not only in CTLL2 cells, but also in mouse Ag-activated primary CD8+ T cells because it rescued functional CD8+ T cells from deprivation induced apoptosis, promoting proliferation in response to subsequent addition of IL-2 or to secondary antigenic challenges. Thus, up-regulation of the CCR2 upon growth factor withdrawal together with the protective effects of CCL2, represent a double-edged survival strategy, protecting cells from apoptosis and enabling them to migrate toward sites where Ag and/or growth factors are available.

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“…The major role of the chemokine system relevant to the context of orthopedic implant pathology includes cell trafficking of immune and inflammatory cells from circulation to the bone–implant interface. Besides its contribution to cell migration ( 3 ), the chemokine system also participates in apoptosis, angiogenesis, tissue repair, and regeneration ( 28 , 31 , 32 ), as well as in the production of collagen ( 33 ). Because of the limited data on other functions of the chemokine system at the bone-implant interface, further studies are needed.…”

Section: The Chemokine System and Its Role In The Periprosthetic Micrmentioning

confidence: 99%

The Role of the Chemokine System in Tissue Response to Prosthetic By-products Leading to Periprosthetic Osteolysis and Aseptic Loosening

2017

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Millions of total joint replacements are performed annually worldwide, and the number is increasing every year. The overall proportion of patients achieving a successful outcome is about 80–90% in a 10–20-years time horizon postoperatively, periprosthetic osteolysis (PPOL) and aseptic loosening (AL) being the most frequent reasons for knee and hip implant failure and reoperations. The chemokine system (chemokine receptors and chemokines) is crucially involved in the inflammatory and osteolytic processes leading to PPOL/AL. Thus, the modulation of the interactions within the chemokine system may influence the extent of PPOL. Indeed, recent studies in murine models reported that (i) blocking the CCR2–CCL2 or CXCR2–CXCL2 axis or (ii) activation of the CXCR4–CXCL12 axis attenuate the osteolysis of artificial joints. Importantly, chemokines, inhibitory mutant chemokines, antagonists of chemokine receptors, or neutralizing antibodies to the chemokine system attached to or incorporated into the implant surface may influence the tissue responses and mitigate PPOL, thus increasing prosthesis longevity. This review summarizes the current state of the art of the knowledge of the chemokine system in human PPOL/AL. Furthermore, the potential for attenuating cell trafficking to the bone–implant interface and influencing tissue responses through modulation of the chemokine system is delineated. Additionally, the prospects of using immunoregenerative biomaterials (including chemokines) for the prevention of failed implants are discussed. Finally, this review highlights the need for a more sophisticated understanding of implant debris-induced changes in the chemokine system to mitigate this response effectively.

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Chemokine Signaling Regulates Apoptosis as well as Immune Cell Traffic in Host Defense

Cited by 9 publications

References 20 publications

Association between decreased CXCL12 and CCL25 expression and increased apoptosis in lymphoid tissues of cynomolgus macaques during SIV infection

Association between decreased CXCL12 and CCL25 expression and increased apoptosis in lymphoid tissues of cynomolgus macaques during SIV infection

CCL2 Inhibits the Apoptosis Program Induced by Growth Factor Deprivation, Rescuing Functional T Cells

The Role of the Chemokine System in Tissue Response to Prosthetic By-products Leading to Periprosthetic Osteolysis and Aseptic Loosening

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