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About CXCL13:

CXCL13, which is short for chemokine (C-X-C motif) ligand 13, is a protein coding gene found in the human body. As the name suggests, it is a part of the CXC chemokine family. It is also known via a variety of other terms. This list includes BLC; BCA1; ANGIE; BCA-1; BLR1L; ANGIE2; and SCYB13. The protein coding gene was first discovered in mice, but scientific understandings have evolved at a rapid rate since.

The CXCL13 protein gene is expressed highly in the liver, spleen, lymph nodes and Peyer’s patches. It promotes the migration of B lymphocytes. CXCL13, as well as the CXCL12 gene, has been shown to be present in demylinating multiple sclerosis lesions, and is elevated in relapsing patients of those conditions. The CXCL13 chemokine gene is linked to CNS immune cells. Cells showing CXCL13 in rheumatoid arthritis and ulcerative colitis are described as monocyte. Malignant cells use CXCL13 resistance to apoptosis and proliferation. The CXCL13 chemokine is chemotactic to cells of the B-1 and B-2 subsets and interacts with the CXCR5 receptor. It acts via BLR1, as is shown by the induced chemotaxis and ca2+ in affected cells. CXCL13 also affects patients with chronic gastritis and gastric lymphomas.

The primary source of CXCL13, in both normal and aberrant lymphoid tissue is, Follicular dendritic cells (FDCs). The monocyte cells produce CXCL13 in lymphoid neogenesis while the presence of C414+ shows a link between CXCL13 and recently extravasated monocytes. CXCL13’s production by FL cells combines with CXCL12 in stromal cells, leading to the accumulation of FL cells in some anatomic areas. CXCL13’s chemical interactions make it an agonist in GTP gamma S binding. It inhibits CTL expansion while testing has shown that the CaM-binding aspects of CXCL13 possesses autohibitory properties. Those chemical changes have been shown in rates to encourage addictive behaviours in rats,and is believed to have similar reactions in humans.

CXCL13 is linked to various therapeutic contests. The coding gene is inhibited by anti-CXCR5 antibodies, wortmannin and pertussis toxin, underlining the genes role in CXCR signalling. Situ hybridization expresses the BCA-1 strand via malignant B cells and, in tumours, is linked to transcytosis. CXCL13 additionally influences the appearance of B cells and T cells in the salivary glands of Sjogren’s syndrome patients and in situ hydration. There is a correlation with viral load, and there is a reduction after HAART (highly active antiretroviral treatment). In analysis, the mRNA levels were 27 times higher in transplants with grouped B cells.

Unlike CXCL12, CXCL13 levels are found to be higher in the OBs of OA patients compared to PT patients. This correlates with the TNF-alpha-stimulated B cells that become chemotaxed. As proven by up regulation of the S100A4 calcium-building gene, CXCL13 additionally induces DNA synthesis and chondrocyte in cartilage explants. BCA1 also interferes with the activity of the FGF-2 growth signalling protein, which means it ma modulate angiogenesis. Alongside CCL19 and CCL22, CXCL13 is present in the third wave, which occurs 24-48 hours later to attract B and T lymphocytes.