MOUSE ANTI HUMAN CD11b Azide Free

Price:
889 EUR
1066 USD
737 GBP
known as: MOUSE ANTI HUMAN CD11b Azide Free
Catalog number: genta-ABS0312
Product Quantity: 1 mg
Category:
Supplier: AbD

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Gene target: cd11b

Related genes to: MOUSE ANTI HUMAN CD11b Azide Free

Symbol : cd11b NIH gene
description : alpha M integrin
type of gene : protein-coding
Modification date : 2015-11-14

Related Pathways to: MOUSE ANTI HUMAN CD11b Azide Free

Related product to: MOUSE ANTI HUMAN CD11b Azide Free

Related Articles about: MOUSE ANTI HUMAN CD11b Azide Free

Upregulation of CD11b and CD86 through LSD1 inhibition promotes myeloid differentiation and suppresses cell proliferation in human monocytic leukemia cells.

LSD1 (Lysine Specific Demethylase1)/KDM1A (Lysine Demethylase 1A), a flavin adenine dinucleotide (FAD)-dependent histone H3K4/K9 demethylase, sustains oncogenic potential of leukemia stem cells in primary human leukemia cells. However, the pro-differentiation and anti-proliferation effects of LSD1 inhibition in acute myeloid leukemia (AML) are not yet fully understood. Here, we report that small hairpin RNA (shRNA) mediated LSD1 inhibition causes a remarkable transcriptional activation of myeloid lineage marker genes (CD11b/ITGAM and CD86), reduction of cell proliferation and decrease of clonogenic ability of human AML cells. Cell surface expression of CD11b and CD86 is significantly and dynamically increased in human AML cells upon sustained LSD1 inhibition. Chromatin immunoprecipitation and quantitative PCR (ChIP-qPCR) analyses of histone marks revealed that there is a specific increase of H3K4me2 modification and an accompanied increase of H3K4me3 modification at the respective CD11b and CD86 promoter region, whereas the global H3K4me2 level remains constant. Consistently, inhibition of LSD1 in vivo significantly blocks tumor growth and induces a prominent increase of CD11b and CD86. Taken together, our results demonstrate the anti-tumor properties of LSD1 inhibition on human AML cell line and mouse xenograft model. Our findings provide mechanistic insights into the LSD1 functions in controlling both differentiation and proliferation in AML. - Source :PubMed

Innate γδT17 cells play a protective role in DSS-induced colitis via recruitment of Gr-1(+)CD11b(+) myeloid suppressor cells.

Innate γδ T cells play critical roles in mucosal immunity such as regulating intestinal epithelial homeostasis. In addition, γδ T cells are significantly increased in the inflamed mucosa of patients with ulcerative colitis. However, γδ T cells are a heterogeneous population. IL-17-producing versus IFNγ-producing γδ T cells play differential roles in different disease settings. Therefore, dissecting the exact role of different subsets of γδ T cells in colitis is essential for understanding colitis immunopathogenesis. In the current study, we found that TCR δ-deficient mice had a more severe dextran sodium sulfate (DSS)-induced colitis that was reduced upon reconstitution of γδT17 cells but not IFNγ-producing γδ T cells. Immunophenotyping of the cellular infiltrate upon DSS-induced colitis showed a reduced infiltration of Gr-1(+)CD11b(+) myeloid cells into the sites of inflammation in mice lacking γδT17 cells. Further experiments demonstrated that IL-17, IL-18, and chemokine CXCL5 were critical in Gr-1(+)CD11b(+) myeloid cell recruitment. In vitro T cell suppressive assay indicated that this Gr-1(+)CD11b(+) population was immunosuppressive. Depletion of Gr-1(+)CD11b(+) myeloid cells resulted in an increase severity of DSS-induced colitis. Our study elucidates a new immune pathway involving γδT17-dependent recruitment of Gr-1(+)CD11b(+) myeloid cells to the site of colitis inflammation important in the protection of colitis initiation and progression. - Source :PubMed

Irf4-dependent CD103(+)CD11b(+) dendritic cells and the intestinal microbiome regulate monocyte and macrophage activation and intestinal peristalsis in postoperative ileus.

Postoperative ileus (POI), the most frequent complication after intestinal surgery, depends on dendritic cells (DCs) and macrophages. Here, we have investigated the mechanism that activates these cells and the contribution of the intestinal microbiota for POI induction. - Source :PubMed

Histamine promotes the differentiation of macrophages from CD11b(+) myeloid cells and formation of foam cells through a Stat6-dependent pathway.

The enzyme histidine decarboxylase (Hdc), which generates histamine, is highly expressed in CD11b(+)Gr-1(+) myeloid cells that play a critical role in infection, inflammation and tumorigenesis. The aim of this study was to explore the role of Hdc-expressing CD11b(+) myeloid cells or histamine in atherogenesis. - Source :PubMed

Different populations of CD11b(+) dendritic cells drive Th2 responses in the small intestine and colon.

T-helper 2 (Th2) cell responses defend against parasites. Although dendritic cells (DCs) are vital for the induction of T-cell responses, the DC subpopulations that induce Th2 cells in the intestine are unidentified. Here we show that intestinal Th2 responses against Trichuris muris worms and Schistosoma mansoni eggs do not develop in mice with IRF-4-deficient DCs (IRF-4(f/f) CD11c-cre). Adoptive transfer of conventional DCs, in particular CD11b-expressing DCs from the intestine, is sufficient to prime S. mansoni-specific Th2 responses. Surprisingly, transferred IRF-4-deficient DCs also effectively prime S. mansoni-specific Th2 responses. Egg antigens do not induce the expression of IRF-4-related genes. Instead, IRF-4(f/f) CD11c-cre mice have fewer CD11b(+) migrating DCs and fewer DCs carrying parasite antigens to the lymph nodes. Furthermore, CD11b(+)CD103(+) DCs induce Th2 responses in the small intestine, whereas CD11b(+)CD103(-) DCs perform this role in the colon, revealing a specific functional heterogeneity among intestinal DCs in inducing Th2 responses. - Source :PubMed

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