Invitrogen™ CCL4 (MIP-1 beta) Human Uncoated ELISA Kit

Description

The Human CCL4 (MIP-1 beta) Uncoated ELISA Kit contains pre-matched antibody pairs,and reagents for performing quantitative enzyme linked immunosorbent assays (ELISA) to detect and quantify protein levels of human CCL4 (MIP-1 beta). Wash Buffer and Stop Solution are needed to complete the ELISA reaction and are sold separately. Principle of the method ELISAs are designed to measure the amount of the target bound between a matched antibody pair. A target-specific antibody is coated to the bottom of the wells of a microplate, which is an overnight process. Samples, standards, or controls are then added into these wells and bind to the immobilized (capture) antibody. A sandwich is formed by the addition of the second (detector) antibody, a substrate solution is added that reacts with the enzyme-antibody-target complex to produce measurable signal. The intensity of this signal is directly proportional to the concentration of target present in the original specimen.

CCL4 (macrophage inflammatory protein 1-beta, MIP1B) belongs to the intercrine beta (chemokine CC) family. Functionally, CCL4 is involved in chemotactic and proinflammatory effects, and homeostasis. CCL4 is produced by macrophages upon stimulation by bacterial endotoxins. CCL4 recruits and stimulates various inflammatory cells at sites of inflammation. CCL4 is produced by lymphocytes, macrophages and dendritic cells. Both CCL4 and the related protein CCL3 participate in the host response to invading bacterial, viral, parasite and fungal pathogens by regulating the trafficking and activation state of selected subgroups of inflammatory cells. While both CCL4 and CCL3 exert similar effects on monocytes, their effect on lymphocytes differ, with CCL4 selectively attracting CD4+ lymphocytes and CCL3 selectively attracting CD8+ lymphocytes. Additionally, both have been shown to be potent chemoattractants for B cells, eosinophils and dendritic cells. The processed form of CCL4 can induce down-modulation of surface expression of the chemokine receptor CCR5, thus inhibiting the CCR5-mediated entry of HIV-1 in T cells. CCL4 binds with high affinity to CCR5 receptors.