CCL18
CCL18 (Chemokine (C-C motif) ligand 18) is a protein that in humans is encoded by the CCL18 gene. This protein is a member of the chemokine family, which are small cytokines or signaling proteins secreted by cells. Chemokines are classified into four main subfamilies: CXC, CC, CX3C, and XC, based on the arrangement of the first two of the four conserved cysteine residues.
Function[edit | edit source]
CCL18 is primarily expressed in lung and lymph node tissues. It is produced by macrophages and dendritic cells in response to inflammatory stimuli. CCL18 plays a significant role in the immune system by attracting T cells, B cells, and natural killer cells to sites of inflammation. It is involved in various immune responses and has been implicated in the pathogenesis of several diseases, including asthma, pulmonary fibrosis, and certain cancers.
Clinical Significance[edit | edit source]
Elevated levels of CCL18 have been associated with idiopathic pulmonary fibrosis (IPF), a chronic and ultimately fatal disease characterized by a progressive decline in lung function. CCL18 is considered a potential biomarker for IPF and other fibrotic diseases. Additionally, high levels of CCL18 have been found in patients with breast cancer, where it may contribute to tumor progression and metastasis.
Gene Location[edit | edit source]
The CCL18 gene is located on chromosome 17 in humans. It is part of a cluster of chemokine genes in this region, which includes other members of the CC chemokine family.
Related Chemokines[edit | edit source]
CCL18 is closely related to other CC chemokines such as CCL3, CCL4, and CCL5. These chemokines share structural similarities and often have overlapping functions in the immune system.
Research and Therapeutic Potential[edit | edit source]
Research into CCL18 is ongoing, with studies focusing on its role in various diseases and its potential as a therapeutic target. Inhibiting CCL18 activity may offer new treatment strategies for conditions like IPF and certain cancers.
See Also[edit | edit source]
References[edit | edit source]
External Links[edit | edit source]
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