An Activating and Inhibitory Signal from an Inhibitory Receptor LMIR3/CLM-1: LMIR3 Augments Lipopolysaccharide Response through Association with FcRγ in Mast Cells

Izawa, Kumi; Kitaura, Jiro; Yamanishi, Yoshihiro; Matsuoka, Takahiro; Kaitani, Ayako; Sugiuchi, Masahiro; Takahashi, Mariko; Maehara, Akie; Enomoto, Yutaka; Oki, Toshihiko; Takai, Toshiyuki; Kitamura, Toshio

doi:10.4049/jimmunol.0900552

Cited by 53 publications

(92 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Two putative ITIMs encompassing Y205 and Y249 have been identified, and a substitution (tyrosine into phenylalanine) analysis revealed that these were required for the CD300F-mediated inhibitory effects (8). However, the action mechanism of CD300F still requires more detailed analysis because cross-linking of mouse CD300F, in contrast to the previously mentioned results, augmented LPS response through its association with FcRg in mast cells (7) and induced apoptotic cell death in human acute myeloid leukemia and myeloid cells (9,10).…”

mentioning

confidence: 42%

“…In experimental autoimmune encephalomyelitis, CD300F expression was detected on inflammatory myeloid cells present in demyelinated areas and the absence of CD300F increased production of the proinflammatory mediators and aggravated the clinical symptoms (5). In addition, cross-linking of CD300F has been shown to inhibit the inflammatory activation of macrophages induced by the stimulation of BAFF, a member of the TNF superfamily (6) and activation of mast cells induced by FcεR stimulation (1,7). Furthermore, overexpression CD300F in RAW264.7 cells inhibited osteoclastogenesis induced by the RANKL, another member of TNF superfamily (3).…”

mentioning

confidence: 99%

See 1 more Smart Citation

CD300F Blocks Both MyD88 and TRIF-Mediated TLR Signaling through Activation of Src Homology Region 2 Domain-Containing Phosphatase 1

Lee

Kim

Suk

et al. 2011

The Journal of Immunology

View full text Add to dashboard Cite

CD300F is known to exhibit inhibitory activity in myeloid cells through its intracellular ITIM. To investigate the effect of CD300F stimulation on TLR signaling, the human acute monocytic leukemia cell line THP-1 was treated with CD300F-specific mAbs or two synthetic peptides that represented the ITIM-like domains of CD300F. Treatment with these agents blocked TLR2-, 3-, 4-, and 9-mediated expression of proinflammatory mediators such as IL-8 and matrix metalloproteinase-9. The luciferase reporter assay in 293T cells and Western blot analysis of THP-1 cells revealed that these inhibitory actions were effective in pathways involving MyD88 and/or TRIF of TLR signaling and associated with marked suppression of IκB kinase activation, phosphorylation/degradation of IκB, and subsequent activation of NF-κB. Use of specific inhibitors and immunoprecipitation analysis further indicated that the inhibitory effects were mediated by Src homology 2 domain-containing phosphatase-1, a protein tyrosine phosphatase with inhibitory activity in hematopoietic cells. These data indicate that CD300F is an active regulator of TLR-mediated macrophage activation through its association with Src homology 2 domain-containing phosphatase-1 and that the synthetic peptides can be applied for the regulation of immune responses that are induced by TLRs.

show abstract

mentioning

confidence: 42%

mentioning

confidence: 99%

CD300F Blocks Both MyD88 and TRIF-Mediated TLR Signaling through Activation of Src Homology Region 2 Domain-Containing Phosphatase 1

Lee

Kim

Suk

et al. 2011

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…Consequently, mouse CD300f has been shown to serve as either an activating or an inhibitory receptor (17,18,(45)(46)(47)(48). Our previous work showed that the CD300f cytoplasmic tail initiates either positive or negative signals for phagocytosis of ACs upon recognition of PS (17).…”

Section: Animals Cd300fmentioning

confidence: 99%

Dendritic cells expressing immunoreceptor CD300f are critical for controlling chronic gut inflammation

Lee¹,

Tian²,

Bouladoux³

et al. 2017

Journal of Clinical Investigation

View full text Add to dashboard Cite

“…The 3 0 UTR was cloned to downstream of the Renilla luciferase stop codon in pGL4.74 vector (Promega, Madison, WI, USA). To generate the mutant 3 0 UTR of the mouse Trp53inp1, two-step PCR mutagenesis was performed [24][25][26] using the WT-3 0 UTR as a template. The Rluc-2 Â 125b site vector contained two copies of a sequence designed to be perfectly complementary to the miR125b downstream of the Renilla luciferase stop codon.…”

Section: Luciferase Assaymentioning

confidence: 99%

Eμ/miR-125b transgenic mice develop lethal B-cell malignancies

et al. 2011

View full text Add to dashboard Cite

MicroRNA-125b-1 (miR-125b-1) is a target of a chromosomal translocation t(11;14)(q24;q32) recurrently found in human B-cell precursor acute lymphoblastic leukemia (BCP-ALL). This translocation results in overexpression of miR-125b controlled by immunoglobulin heavy chain gene (IGH) regulatory elements. In addition, we found that six out of twenty-one BCP-ALL patients without t(11;14)(q24;q32) showed overexpression of miR-125b. Interestingly, four out of nine patients with BCR/ABL-positive BCP-ALL and one patient with B-cell lymphoid crisis that had progressed from chronic myelogenous leukemia overexpressed miR-125b. To examine the role of the deregulated expression of miR-125b in the development of B-cell tumor in vivo, we generated transgenic mice mimicking the t(11;14)(q24;q32) (El/miR-125b-TG mice). El/miR-125b-TG mice overexpressed miR-125b driven by IGH enhancer and promoter and developed IgM-negative or IgM-positive lethal B-cell malignancies with clonal proliferation. B cells obtained from the El/miR-125b-TG mice were resistant to apoptosis induced by serum starvation. We identified Trp53inp1, a proapoptotic gene induced by cell stress, as a novel target gene of miR-125b in hematopoietic cells in vitro and in vivo. Our results provide direct evidence that miR-125b has important roles in the tumorigenesis of precursor B cells.

show abstract

An Activating and Inhibitory Signal from an Inhibitory Receptor LMIR3/CLM-1: LMIR3 Augments Lipopolysaccharide Response through Association with FcRγ in Mast Cells

Cited by 53 publications

References 45 publications

CD300F Blocks Both MyD88 and TRIF-Mediated TLR Signaling through Activation of Src Homology Region 2 Domain-Containing Phosphatase 1

CD300F Blocks Both MyD88 and TRIF-Mediated TLR Signaling through Activation of Src Homology Region 2 Domain-Containing Phosphatase 1

Dendritic cells expressing immunoreceptor CD300f are critical for controlling chronic gut inflammation

Eμ/miR-125b transgenic mice develop lethal B-cell malignancies

Contact Info

Product

Resources

About