Role of CD69 in acute lung injury

Ishizaki, Shunsuke; Kasuya, Yoshitoshi; Kuroda, Fuminobu; Tanaka, Kensuke; Tsuyusaki, Junichi; Yamauchi, Keita; Matsunaga, Hirofumi; Iwamura, Chiaki; Nakayama, Toshinori

doi:10.1016/j.lfs.2012.03.018

Cited by 13 publications

(11 citation statements)

References 34 publications

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“…By contrast, to the best of our knowledge, this is the first report which shows a clear relationship between inflammatory/immune infiltrates and tumor cytogenetics in meningiomas. Overall, meningiomas carrying isolated monosomy 22/del(22q) showed significantly greater numbers of TiMa infiltrating the tumor, together with a more pronounced activation profile of immune cells, as reflected by greater percentages of CD69 + and CD63 + TiMa and/or lymphocytes [22], [23], versus cases with either a diploid or a complex iFISH karyotype. In addition, HLA-DR + CD14 + CD45 + CD68 + TiMa from patients with isolated monosomy 22/del(22q) also showed higher levels of expression of CD16, an FcγRIII receptor typically absent in recently produced blood monocytes, but expressed during macrophage maturation in peripheral tissues (e.g.…”

Section: Discussionmentioning

confidence: 95%

Association between Inflammatory Infiltrates and Isolated Monosomy 22/del(22q) in Meningiomas

et al. 2013

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Meningiomas contain highly variable levels of infiltrating tissue macrophages (TiMa) and other immune cells. In this study we investigated the potential association between the number and immunophenotype of inflammatory and other immune cells infiltrating the tumor as evaluated by multiparameter flow cytometry, and the clinico-biological, cytogenetic and gene expression profile (GEP) of 75 meningioma patients. Overall, our results showed a close association between the amount and cellular composition of the inflammatory and other immune cell infiltrates and the cytogenetic profile of the tumors. Notably, tumors with isolated monosomy 22/del(22q) showed greater numbers of TiMa, NK cells and (recently)-activated CD69+ lymphocytes versus meningiomas with diploid and complex karyotypes. In addition, in the former cytogenetic subgroup of meningiomas, tumor-infiltrating TiMa also showed a more activated and functionally mature phenotype, as reflected by a greater fraction of CD69+, CD63+, CD16+ and CD33+ cells. GEP at the mRNA level showed a unique GEP among meningiomas with an isolated monosomy 22/del(22q) versus all other cases, which consisted of increased expression of genes involved in inflammatory/immune response, associated with an M1 TiMa phenotype. Altogether, these results suggest that loss of expression of specific genes coded in chromosome 22 (e.g. MIF) is closely associated with an increased homing and potentially also anti-tumoral effect of TiMa, which could contribute to explain the better outcome of this specific good-prognosis cytogenetic subgroup of meningiomas.

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Section: Discussionmentioning

confidence: 95%

Association between Inflammatory Infiltrates and Isolated Monosomy 22/del(22q) in Meningiomas

et al. 2013

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“…Global miRNA profile analysis showed that the expression of miR-155 was elevated in ALI (21,23). Furthermore, miR-155 could regulate the transduction of TLRs signaling on mouse and human immune cells such as macrophages (24,25), *Department of Respiratory Medicine, East Hospital, Tongji University School of Medicine, Shanghai, China; which was critical for generation of proinflammatory cytokine storm and subsequently the development and recovery of ALI (26)(27)(28). Of interest, one report showed that pretreatment of antisense oligonucleotides (ASO) against miR-155 could lead to decreased expression of GM-CSF, which was an important pathogenetic factor in the pathology of ALI in LPS induced animal inflammatory disease (29).…”

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confidence: 99%

Antisense Oligonucleotide Treatment Enhances the Recovery of Acute Lung Injury through IL-10–Secreting M2-like Macrophage-Induced Expansion of CD4+ Regulatory T Cells

Guo

Wen

Qin

et al. 2013

The Journal of Immunology

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MicroRNAs (miRNAs) have been shown as an important regulator in the pathologies of acute lung injury (ALI). However, the potential effect of miRNA-based therapeutic studies in ALI remains poorly understood. We assessed the effect of antisense oligonucleotides (ASOs) against miR-155 on the development of ALI using a murine ALI model. We found that miR-155 ASO treatment could enhance the recovery of ALI as evidenced by accelerated body weight back, reduced level of bronchoalveolar lavage (BAL) protein and proinflammatory cytokines, and reduced number of BAL cells. Adoptive cell transfer assay in RAG1−/− mice showed that CD4+CD25+ regulatory T cells (Tregs) mediated the enhanced recovery of ALI. Mechanistic evidence showed that enhanced expansion of Tregs in vivo, dominantly induced by IL-10–secreting M2-like macrophages, was critical for their elevated proportion in miR-155 ASO-treated ALI mice. Finally, we report that C/EBPβ, a target molecule of miR-155, was upregulated and associated with IL-10 secretion and M2-like phenotype of macrophages. These data provided a previously unknown mechanism for miRNA-based therapy against ALI, which could ultimately aid the understanding of recovery of ALI and the development of new therapeutic strategies against clinical inflammatory lung disease.

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“…MIP2 and MCP1 are two immune response chemokines. In acute reactions, these proteins can induce chemotaxis of monocytes, macrophages, and neutrophils to the sites of inflammatory lesions [12,13], which is additionally involved in the acute inflammatory process [14,15].…”

Section: Discussionmentioning

confidence: 99%

CUEDC2 Protects Against Experimental Colitis and Suppresses Excessive Proliferation of Intestinal Mucosa

Wang

et al. 2015

Dig Dis Sci

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Role of CD69 in acute lung injury

Cited by 13 publications

References 34 publications

Association between Inflammatory Infiltrates and Isolated Monosomy 22/del(22q) in Meningiomas

Association between Inflammatory Infiltrates and Isolated Monosomy 22/del(22q) in Meningiomas

Antisense Oligonucleotide Treatment Enhances the Recovery of Acute Lung Injury through IL-10–Secreting M2-like Macrophage-Induced Expansion of CD4+ Regulatory T Cells

CUEDC2 Protects Against Experimental Colitis and Suppresses Excessive Proliferation of Intestinal Mucosa

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