Overview
- Peptide RLDNYNDTSLVENHLC, corresponding to amino acid residues 23-38 of human CXCR5 (Accession P32302). Extracellular, N-terminus.
- Burkitt's lymphoma (Raji), human prostate carcinoma (LNCaP and PC-3) cell lines (1:400-1:2000).
- Western blot analysis of Burkitt's lymphoma (Raji) (lanes 1 and 4), human prostate carcinoma (LNCaP) (lanes 2 and 5) and human prostate carcinoma (PC-3) cell line lysates (lanes 3 and 6):1-3. Anti-Human CXCR5 (extracellular) Antibody (#ACR-015), (1:400).
4-6. Anti-Human CXCR5 (extracellular) Antibody, preincubated with Human CXCR5 (extracellular) Blocking Peptide (#BLP-CR015).
- Human promyelocytic leukemia (HL-60) cell line (5 μg/0.5x106 cells).
- Human prostate carcinoma (LNCaP) live intact cells (1:25).
Chemokine receptors are a family of receptors that signal upon binding of one or more members of the chemokine superfamily of chemotactic cytokines. Chemokines coordinate development, differentiation and trafficking of various immune system cells making them key players of the innate and adaptive immune response.
CXCR5 (also known as Burkitt lymphoma receptor 1) belongs to the CXC subfamily of chemokine receptors and is a G-coupled protein receptor with 7 transmembrane segments. There is considerable homology between CXCR5 and other members of the chemokine receptor family such as IL-9 receptor, CCR-1 and BLR2. CXCR5 expression is detected in peripheral blood CD4 and CD8 leukocytes as well as in secondary lymphatic organs and in granule and Purkinje layers in the brain. It is also expressed in Burkitt’s lymphoma cells1.
CXCR5 is activated by B-cell attracting chemokine 1 (BCA-1) that is chemotactic for human B lymphocytes. BCA-1 does not affect IL-2 stimulated T-cells, monocytes or neutrophils2. CXCR5 mediates correct T cell localization within granulomas, efficient macrophage activation and lymphoid follicle formation3.
CXCR5 knockout mice have a severe defect in normal B cell migration and localization. Knockout mice lack inguinal lymph nodes, have a reduced amount of Peyer’s patches and have abnormal primary lymphoid follicles and no functional germinal centers in the spleen4. Absence of CXCR5 has been implicated in increased susceptibility to tuberculosis to due defective T cell localization within the lung3.