TIM-4 Rat anti-Mouse, PE, Clone: 54 (RMT4-54), eBioscience™

Description

Description: The monoclonal antibody 54 recognizes mouse Tim-4 (T cell, Ig, mucin). Unlike other Tim family members, Tim-4 is not expressed on T lymphocytes but rather found on antigen presenting cells such as lymphoid and myeloid DC′s and macrophages. Tim-4 has been shown to interact with Tim-1 thereby suggesting a role of Tim-4 in the balance of Th1/Th2 regulation. Additionally Tim-4 has been shown to be a receptor for phosphatidylserine and may play a role in engulfment of apoptotic cells. Expression is found on a subset of CD11c+ splenic cells. Applications Reported: This 54 (RMT4-54) antibody has been reported for use in flow cytometric analysis. Applications Tested: This 54 (RMT4-54) antibody has been tested by flow cytometric analysis of mouse splenocytes. This can be used at less than or equal to 0.25 µg per test. A test is defined as the amount (µg) of antibody that will stain a cell sample in a final volume of 100 µL. Cell number should be determined empirically but can range from 10^5 to 10^8 cells/test. It is recommended that the antibody be carefully titrated for optimal performance in the assay of interest. Please consider the use of a viability dye like 7-AAD (cat 00-6993) when staining for Tim4. Excitation: 488-561 nm; Emission: 578 nm; Laser: Blue Laser, Green Laser, Yellow-Green Laser. Filtration: 0.2 μm post-manufacturing filtered.

The T cell immunoglobulin and mucin domain containing protein (TIM) family encodes cell surface receptors that are involved in the regulation of T helper (Th) -1 and -2 cell-mediated immunity. TIM-4, which is preferentially expressed on macrophages and dendritic cells, is the natural ligand of TIM-1, and this binding leads to T-cell expansion and cytokine production. Unlike other members of the TIM family, TIM-4 lacks a putative tyrosine phosphorylation signal sequence in its intracellular domain. The TIM-4 gene maps to a locus associated with predisposition to asthma in both mice and humans and with its connection to TIM-1-triggered Th2 responsiveness, may be considered as a candidate disease/predisposition gene for asthma.