About InVivoMAb anti-mouse TIM-4 The F31-5G3 monoclonal antibody reacts with mouse T cell immunoglobulin and mucin domain 4 (TIM-4) a phosphatidylserine-binding receptor and member of the Ig superfamily. TIM-4 is preferentially expressed on antigen-presenting cells. TIM-4 is thought to enhance the engulfment of apoptotic cells and play a role in regulating T cell proliferation. InVivoMAb anti-mouse TIM-4 Specifications IsotypeRat IgG1, κ Recommended Isotype Control(s)InVivoMAb rat IgG1 isotype control, anti-horseradish peroxidase Recommended Dilution BufferInVivoPure pH 7.0 Dilution Buffer ImmunogenMouse TIM4-Ig fusion protein Reported ApplicationsFlow cytometry FormulationPBS, pH 7.0 Contains no stabilizers or preservatives Endotoxin<2EU/mg (<0.002EU/μg) Determined by LAL gel clotting assay Purity>95% Determined by SDS-PAGE Sterility0.2 μm filtration ProductionPurified from cell culture supernatant in an animal-free facility PurificationProtein G RRIDAB_2894763 Molecular Weight150 kDa StorageThe antibody solution should be stored at the stock concentration at 4°C. Do not freeze. Application ReferencesInVivoMAb anti-mouse TIM-4 (CLONE: F31-5G3)Seidman, J. S., et al (2020). "Niche-Specific Reprogramming of Epigenetic Landscapes Drives Myeloid Cell Diversity in Nonalcoholic Steatohepatitis" Immunity 52(6): 1057-1074 e1057. PubMedTissue-resident and recruited macrophages contribute to both host defense and pathology. Multiple macrophage phenotypes are represented in diseased tissues, but we lack deep understanding of mechanisms controlling diversification. Here, we investigate origins and epigenetic trajectories of hepatic macrophages during diet-induced non-alcoholic steatohepatitis (NASH). The NASH diet induced significant changes in Kupffer cell enhancers and gene expression, resulting in partial loss of Kupffer cell identity, induction of Trem2 and Cd9 expression, and cell death. Kupffer cell loss was compensated by gain of adjacent monocyte-derived macrophages that exhibited convergent epigenomes, transcriptomes, and functions. NASH-induced changes in Kupffer cell enhancers were driven by AP-1 and EGR that reprogrammed LXR functions required for Kupffer cell identity and survival to instead drive a scar-associated macrophage phenotype. These findings reveal mechanisms by which disease-associated environmental signals instruct resident and recruited macrophages to acquire distinct gene expression programs and corresponding functions.Takasato, Y., et al (2020). "Orally desensitized mast cells form a regulatory network with Treg cells for the control of food allergy" Mucosal Immunol . PubMedOral immunotherapy (OIT) is an effective approach to controlling food allergy. Although the detailed molecular and cellular mechanisms of OIT are unknown currently, they must be understood to advance the treatment of allergic diseases in general. To elucidate the mechanisms of OIT, especially during the immunological transition from desensitization to allergy regulation, we generated a clinical OIT murine model and used it to examine immunological events of OIT. We found that in mice that completed OIT successfully, desensitized mast cells (MCs) showed functionally beneficial alterations, such as increased induction of regulatory cytokines and enhanced expansion of regulatory T cells. Importantly, these regulatory-T-cell-mediated inhibitions of allergic responses were dramatically decreased in mice lacking OIT-induced desensitized MC. Collectively, these findings show that the desensitization process modulates the activation of MCs, leading directly to enhanced induction of regulatory-T-cell expansion and promotion of clinical allergic unresponsiveness. Our results suggest that efficiently inducing regulatory MCs is a novel strategy for the treatment of allergic disease.
