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We validate the specificity of these antibodies to C-C motif chemokine 2 by testing them on tissues known to express CCL2 positively and negatively. Browse below to find the CCL2 antibody that suites your experiment. We have 13 of these antibodies and many publications and validation images.
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Facts about C-C motif chemokine 2.
Has been implicated in the pathogenesis of diseases characterized by monocytic infiltrates, like psoriasis, rheumatoid arthritis or atherosclerosis. May be involved in the recruitment of monocytes into the arterial wall during the disease process of atherosclerosis.
|intercrine beta (chemokine CC) family|
C-C motif chemokine ligand 2; CCL2; GDCF-2; HC11; HSMCR30; MCAF; Mcp1; MCP-1; SCYA2; SMC-CF
|Sequence:||17; NC_000017.11 (34255285..34257203)|
Expressed in the seminal plasma, endometrial fluid and follicular fluid (at protein level).
This article will provide an overview of CCL2's effects on myeloid, dendritic and macrophage polarization and T cell function. This article will teach you how you can use the gene to test different biological processes. In addition, we'll explore the implications of the use of this gene in cancer research. CCL2 is likely to play a part in your research, regardless of whether you're in academia or in the pharmaceutical industry.
CCL2's function in myeloid cell proliferation and phenotype is still not fully understood. It may play multiple functions in immune cells. It is being investigated in detail to determine its precise role in these processes. However, a variety of evidence suggest CCL2 is involved in myeloid cell function. It is known to upregulate antiapoptotic protein, inhibit the caspases-3 and -8 that are crucial for CD11b+ cell survival. Additionally, it regulates NFAT5, a transcription factor involved in the response to hypoxic and proinflammatory stimuli.
We're not able to fully comprehend the molecular mechanisms CCL2 has on myeloid cells. While it is believed to promote tumor growth however, it also blocks immune responses. CCL2 affects the function of myeloid cell function and increases the recruitment of T cells to tumors. Tumors can benefit from this effect by enhancing angiogenesis as well as inhibiting other immune cells.
CCL2 was discovered to increase the rate of efferocytosis in macrophages. It also increased apoptotic cell destruction. After treatment with CCL2, human neutrophils were cocultured in a study with Recombinant CCL2. Researchers stained macrophages using Diff Quik to look for cells that had died. These macrophages were injected into mice who received CCL2.
Numerous studies have demonstrated that CCL2 has distinct effects on myeloid cells from various cancers. CCL2's diverse effects on myeloid cells could be the reason why many treatments which target this chemotherapeutic factor do not work. Understanding the molecular mechanisms that govern CCL2 function could reveal the potential explanations. The authors highlight several important aspects of CCL2 biology that warrant further investigation.
In addition to its cytotoxic capabilities, CCL2 has been shown to reduce the proliferation of neutrophils. CCL2 is exogenous and causes tumor-neutrophil cytotoxicity in naive neutrophils. However the addition of an anti-CCL2 antibodies decreased cytotoxicity of naive neutrophils. CCL2 was also detected in naive neutrophils which resulted into significantly less lung metastases in mice.
The effect of CCL2 on dendritic cells is well-known however, what exactly does it do? This compound binds to CCR4 receptor on regulatory T cells, or Tregs. These cells are drawn to the tumor through the chemokine. Thus, blocking its production can prevent growth of the tumor and infiltration by Tregs. CCL22 is expressed by dendritic cells stimulated by the IL-1alpha receptor, which decreases Treg recruitment.
A study of the interaction of HBEC and monocyte-derived dendritic cells showed that HBEC stimulates the T1 polarisation reaction in dendritic cells. In contrast, cHBEC and saHBEC induced an evident increase in CD80 and CD86 in moDC. In addition, cHBEC is able to cause upregulation of both CD40 and CD80 in dendritic cells.
By employing a cell culture method based on transfection, the T cells that were naive were treated with CCL2 for 30 min and then stimulated with 100 ng/mL of CCL21 for 1 to 2.5 minutes. The lysates were later separated by SDS-PAGE and the immunoblots were made using an anti-phosphospecific antibody. The transfected cells were washed and immunoblotted with a PE-conjugated secondary Ab to detect the phosphorylated proteins.
Similar to that, CCL2 does not promote T-cell activation. However, its levels in circulation are elevated in various situations of inflammation. Moreover, CCL2 may trigger a negative feedback mechanism that inhibits T-cell activation in various inflammation processes. However, at the conclusion of the inflammation process, low levels of CCL2 hinder the entry of naive and central memory T cells into the LN.
Other studies have shown that CCL2 has a dual impact on dendritic cells. In transgenic mice, CCL2 significantly reduces the capacity of CCR2-/ lymphocytes to adhere to wall of the HEV. It is not clear if CCL2 inhibits CCR2 receptors or has an effect on the production of protein. These results suggest that CCL2 could play a role in neuroinflammation and synaptic transmission.
The chemical chemokine CCL2 influences the release neurotransmitters from the brain. By regulating this hormone it affects neuronal activity synaptic responses, as well as ion channel function. It co-localizes in the substantianigral cortex along with dopamine, acetylcholine and other hormones. CCL2 plays a role in the interaction of neural cells and glia, in addition to its immunomodulatory properties.
The CCL2/CCR2-axis regulates the recruitment of monocytes to infection sites and the egress of bone marrow. Understanding the mechanisms that regulate CCL2/CCR2 expression can help identify new therapeutic targets for autoimmune and inflammation diseases. It is interesting to consider that proinflammatory and antiinflammatory macrophages express different CCL2/CCR2 profiles. Activin A increases CCR2 expression in macrophages which causes them to shift their polarization.
Macrophage polarization is influenced by the role of NFkB's transcriptional activity in regulation of M1–M2 switch. The regulation of macrophage-polarization plays the primary function of SOCS1 and STAT1 proteins of the NF-kB family. These proteins are essential to maintaining a proinflammatory phenotype throughout a variety of biological processes, like Eosinophil migration and granule movement.
While the mechanisms for regulation of macrophage polarization may be complicated There is clear evidence that multiple factors influence their plasticity. The significance of the monocyte subset in the repair of tissues after inflammation is compelling. This indicates that monocytes' regenerative capacity is prior to that of macrophages. This study also indicates that CCL2 is essential to control macrophage-polarization.
STAT-3, STAT-6 play a critical role in anti-inflammatory M2 macrophage and macrophage polarization. Actually, STAT-3 regulates pro-inflammatory NF kB pathways, which then regulates IRF-3 that is anti-inflammatory. These two proteins, in conjunction with other proteins control macrophage polarization. They also influence the IFN-g signaling, and IL-10 production.
In a recent study we used bone marrow-derived murine macrophages from WT mice and Ccr2 mice. CCR2 expression was higher in CCL2-/ mice than in mouse macrophages that were GM-MO. Although mice without CCR2 showed lower M1/M2 ratios, the absence of CCR2 significantly affected the ratio of M1 and M2 macrophages within the mouse peritoneum. Furthermore, mice lacking Ccr2 were without CD11bhigh F4/80int M2 macrophages, thereby altering the expression of polarization markers.
Mphs with different polarization states have distinct protective effects on MM cells. CCL2 increases Mphs' protective effects by polarizing them towards an M2-like appearance. This is associated with changes in the intrinsic chemistry of MM cells and their chemoresistance. In addition, Mphs are important components of the BM microenvironment, and play an important role in defending MM cells from apoptosis induced by drugs.
CCL2's function within the immune system is not fully comprehended. Its primary function is to stimulate the migration of myeloid and lymphocytes in the presence of pathological conditions. Its effects can be utilized to influence immune cells' polarization and to regulate the production of IL-10 and IL-12. We review several studies that examined the role CCL2 plays in the immune system.
CCL2 is an important factor in the biology of monocytes and macrophages. It affects the maturation and differentiation of monocytes into DCs or MDSCs. DCs move to lymphoid organs , and then present foreign material to T cells. The function of T cells was affected by activation of these cell types by ligands such CD40L or IL-4. They also showed different responses to IL-32 and IFNg.
A study conducted using mice with CCL2-deficient CCL failed to demonstrate enhanced immunogenicity in tumor-derived CCL2 cells in comparison to CCL2+ cells. In contrast, CCL2-deficient cells display decreased immunogenicity, suggesting that tumor-derived CCL2 interferes with the effector functions of T cells. Additionally, tumors that are depleted in CCL2 reduce the immune-genicity of the tumor.
Other studies have shown that CCL2 can influence polarization of macrophages. CCL2 can cause a macrophage to become more M2-type if it is provided. It can also alter the polarization and function of immune cells like T cells. However, more research is required to determine the exact function of CCL2 in the immune response. This mechanism of CCL2 however is highly dependent on the context.
Although the CCL2 receptor remains controversial Numerous scientists have discovered that microglia express this protein and it is crucial for the inflammation response. CCR2 plays multiple roles in inflammation, such as activating microglia. The expression of CCR2 is also linked to pain-related functions in neurons, such as DRG neurons as well as second-order neuronal cells in lamina II.
In cancer, CCL2 and CCR2 have been linked to increased malignancy. These molecules play an important role in angiogenesis, cell movement, and metastasis. CCR2 levels in human cancer cells are associated with a higher incidence of prostate cancer. Both could be therapeutic targets for cancer. More research is needed to determine whether CCR2 is associated with PCa.
*Showing only the more recent 20. More publications can be found for each product on its corresponding product page