C-C motif chemokine 22 Antibodies

C-C motif chemokine 22 (CCL22)

May play a role in the trafficking of activated/effector T-lymphocytes to inflammatory sites and other facets of actuated T-lymphocyte physiology. Chemotactic for monocytes, dendritic cells and natural killer cells.

Mild chemoattractant for primary activated T-lymphocytes and a potent chemoattractant for chronically activated T-lymphocytes but doesn't have chemoattractant activity for neutrophils, eosinophils, and resting T-lymphocytes. Binds to CCR4.

Gene Information

Human
Gene Name:	CCL22
Uniprot:	O00626
Entrez:	6367

Family

Belongs to:
intercrine beta (chemokine CC) family

Alternative Names

A-152E5.1; ABCD-1; CC chemokine STCP-1; C-C motif chemokine 22; CCL22; chemokine (C-C motif) ligand 22; DC/B-CK; Macrophage-derived chemokine; MDC; MDCStimulated T-cell chemotactic protein 1; MGC34554; SCYA22MDC(1-69); small inducible cytokine A22; small inducible cytokine subfamily A (Cys-Cys), member 22; Small-inducible cytokine A22; STCP-1; stimulated T cell chemotactic protein 1

Molecular Weight

Mass (kDA):
10.625 kDA

Genomic Context

Human
Location:	16q21
Sequence:	16; NC_000016.10 (57358783..57366189)

Tissue Specificity

Highly expressed in macrophage and in monocyte-derived dendritic cells, and thymus. Also found in lymph node, appendix, activated monocytes, resting and activated macrophages. Lower expression in lung and spleen. Very weak expression in small intestine. In lymph node expressed in a mature subset of Langerhans' cells (CD1a+ and CD83+). Expressed in Langerhans' cell histiocytosis but not in dermatopathic lymphadenopathy. Expressed in atopic dermatitis, allergic contact dermatitis skin, and psoriasis, in both the epidermis and dermis.

Subcellular Localizations

Secreted.

Diseases

• Inflammation
• Cholangiocarcinoma
• Neoplasms
• Asthma
• Dermatitis
• Dermatitis, Atopic
• Malignant Neoplasms
• Carcinoma
• Autoimmune Reaction
• Dermatologic Disorders
• Tissue Adhesions
• Lymphoma
• Allergy

• Pneumonia
• Eosinophilia
• Hiv Infections
• Malignant Paraganglionic Neoplasm
• Leukemia
• Inflammatory Response
• Decreased Immunologic Activity [pe]

Pathways

• Pathogenesis
• Secretion
• Immune Response
• Chemotaxis
• Chemokine Production
• Sensitization
• Cell Migration
• Inflammatory Response
• Cell Proliferation
• Localization
• Cell Activation
• T Cell Proliferation
• Cytokine Production

• Hypersensitivity
• T Cell Activation
• Cytokine Secretion
• Cell Differentiation
• Platelet Aggregation
• Phagocytosis
• Platelet Activation

PTMs

• Phosphorylation
• Cleavage
• Oxidation
• Acetylation

• Nitration
• Biotinylation
• Methylation
• Prenylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/CCL22

Boster Bio: Best Uses Of The CCL22 Marker

CCL22 is secreted in many tissues and tumors. Therefore, researchers are interested to know how this can be used to identify their potential clinical uses. This article will discuss this novel molecule and its use in biology. It not only demonstrates the biomarker's clinical applications, but also shows how synthetic CCL22 is possible for human trials.

Many tumors secrete CCL22.

CCL22 is secreted mainly by tumors. However, it's still unclear what the protein does. Although it plays a vital role in the development of several types of cancer, few studies have been conducted on the protein's role in malignancy. Recent research by Li and al. Recent research by Li, et al. It is a factor in the migration of activated T, NK and monocyte-derived dermritis cells. It is also a chemoattractant of regulatory T cells.

In a study, CCL22 levels were measured in plasma, peritoneal and tissue. The authors found that plasma and peritoneal fluid samples from women with ovarian cancer contained significantly higher levels of CCL22 than those of women with benign ovarian disease. In the same way, plasma CCL22 levels in women with stage IV FIGO were significantly higher than those from women without cancer. However, these results were not statistically significant.

Although tumor-associated CCL22 was shown to play a role during the development of certain types of cancers, research into nTreg cells involved in prostate cancer remains incomplete. However, evidence suggests that tumors may produce CCL22 in response to an antigen-presenting cell. Because CCL22 is secreted by many tumors, the role of this protein in the development of cancer remains unclear.

CCL17 is released by cancer cells, as well as CCL22 and CCL22. These secretions recruit Treg cell to the microenvironment. These findings indicate that tumor-associated macrophages play a role in the development of cancer. CCR4 positive cancer cells migrate to and from the lung more often than others. Further, prostate cancer cells that express CCR4 are also associated with lung metastasis.

While tumor-associated chemokines have been found to be important for cancer immunotherapy, CCL22 is a novel factor for tumor-related immunity. CCL22 can be produced by tumor-associated microphages which recruit T(reg). The immune system is able to fight tumors faster by early detection of tumor cells. CCL22 has a variety of other effects on the growth of cancerous cells in different tissues.

TAMs' extracellular matrix helps cancer cells resist radiotherapy or chemotherapy. They also influence the interaction between cancer cells and macrophages. These TAMs can be targeted for molecular therapy. It is a very effective factor in cancer related TAMs. TAMs may contribute to tumor growth, but more research is needed.

It is secreted through foreign tissue

The CCL22 mark is secreted primarily by macrophages. These are versatile immune cell types that respond to various microenvironmental signaling. Chemokines belong to the CC chemokine family. They act as cell chemotactic factor. They have recently added a new dimension to transcriptional profiling. This marker is derived mostly from macrophages, and is usually labeled type-M2 macrophage. It promotes tumor cell migration and correlates well with venous infiltrates. It is secreted by type M2 macrophages. It promotes tumor formation, correlates with vein infiltration, and selectively recruits CCR4+-T lymphocytes.

Fucoidan was found to induce CCL22 in M2 macrophages. Fucoidan significantly inhibited the transcription of CCL22 in M2 macrophages, and reduced the ability of these cells to migrate toward a foreign tissue. CCL22 neutralizing Abs impeded M2 macrophages from migrating, while rhCCL22 significantly boosted the migration capability of MHCC97H.

Fucoidan inhibits CCL22 transcription in peripheral blood mammaphages. CCL22 was elevated in vitro during differentiation of monocytes into M0, M1 macrophages using IL-4 or IL-13. CCL22 production was also stimulated in M2-like macrophages by IL-4. Fucoidan, a powerful antiviral agent, has synergistic interactions with IL-13.

Fucoidan inhibits CCL22 in THP-1 THP-1 acute monocyte-leukemia cell line derived microphages. Fucoidan suppresses CCL22 expression in M2 macrophages via NF-kB. In vivo, the anti-tumor properties of fucoidan have yet to be established. However, fucoidan has been shown to inhibit tumor growth and CCL22 production by T-lymphocytes.

It can also be used to indicate potential clinical uses

A CCL22-based marker can be used for clinical purposes. Multiplex assays are used to detect the CCL22 marker within serum and CSF. This marker correlates with several CSF standard parameters and immune cell subsets. CCL22 cannot be used as a clinical indicator yet. More research is needed. Read on to learn more about the potential for this marker.

The CCL22 marker is used to identify microparticles releasing CCL22. These microparticles can reduce bone resorption, and also reduce inflammation in cells. They are therefore useful in identifying promising candidates to be used in clinical trials. Despite these risks and potential dangers, clinical trials have demonstrated promising results. CCL22-releasing microparticles have been shown to be effective in reducing bone resorption, inflammation, and other symptoms.