About InVivoMAb anti-mouse TCR Vγ1.1/Cr4 The 2.11 monoclonal antibody reacts with an epitope in the Cr4 domain of TCR Vγ1.1 (T cell receptor V gamma 1.1). The TCR is expressed on the surface of T lymphocytes and is responsible for recognizing fragments of antigen as peptides bound to MHC molecules. When the TCR engages with antigenic peptide and MHC the T lymphocyte is activated through signal transduction. The Vγ1Jγ4Cγ4 chain is expressed by a major population of γδ T cells in the thymus and peripheral lymphoid organs of adult mice. However, during postnatal and early life stages only a minor population of γδ T cells express Vγ1Jγ4Cγ4 during fetal and early postnatal life. InVivoMAb anti-mouse TCR Vγ1.1/Cr4 Specifications IsotypeArmenian hamster IgG Recommended Isotype Control(s)InVivoMAb polyclonal Armenian hamster IgG Recommended Dilution BufferInVivoPure pH 7.0 Dilution Buffer Immunogen3.13.1 T cell hybridoma Reported Applicationsin vivo Vγ1 TCR+ cell depletion Flow 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 filtered ProductionPurified from cell culture supernatant in an animal-free facility PurificationProtein G RRIDAB_2687736 Molecular Weight150 kDa StorageThe antibody solution should be stored at the stock concentration at 4°C. Do not freeze. Application ReferencesInVivoMAb anti-mouse TCR Vγ1.1/Cr4 (CLONE: 2.11)Zheng, L., et al (2017). "Recruitment of Neutrophils Mediated by Vγ2 γδ T Cells Deteriorates Liver Fibrosis Induced by Schistosoma japonicum Infection in C57BL/6 Mice" Infect Immun 85(8). PubMedConventional adaptive T cell responses contribute to the pathogenesis of Schistosoma japonicum infection, leading to liver fibrosis. However, the role of gamma-delta (γδ) T cells in this disease is less clear. γδ T cells are known to secrete interleukin-17 (IL-17) in response to infection, exerting either protective or pathogenic functions. In the present study, mice infected with S. japonicum are used to characterize the role of γδ T cells. Combined with the infection of S. japonicum, an extremely significant increase in the percentage of neutrophils in the CD45(+) cells was detected (from approximately 2.45% to 46.10% in blood and from 0.18% to 7.34% in spleen). Further analysis identified two different γδ T cell subsets that have different functions in the formation of granulomas in S. japonicum-infected mice. The Vγ1 T cells secrete gamma interferon (IFN-γ) only, while the Vγ2 T cells secrete both IL-17A and IFN-γ. Both subtypes lose the ability to secrete cytokine during the late stage of infection (12 weeks postinfection). When we depleted the Vγ2 T cells in infected mice, the percentage of neutrophils in blood and spleen decreased significantly, the liver fibrosis in the granulomas was reduced, and the level of IL-17A in the serum decreased (P < 0.05). These results suggest that during S. japonicum infection, Vγ2 T cells can recruit neutrophils and aggravate liver fibrosis by secreting IL-17A. This is the first report that a subset of γδ T cells plays a partial role in the pathological process of schistosome infection.Narayan, K., et al (2012). "Intrathymic programming of effector fates in three molecularly distinct gammadelta T cell subtypes" Nat Immunol 13(5): 511-518. PubMedInnate gammadelta T cells function in the early phase of immune responses. Although innate gammadelta T cells have often been studied as one homogenous population, they can be functionally classified into effector subsets on the basis of the production of signature cytokines, analogous to adaptive helper T cell subsets. However, unlike the function of adaptive T cells, gammadelta effector T cell function correlates with genomically encoded T cell antigen receptor (TCR) chains, which suggests that clonal TCR selection is not the main determinant of the differentiation of gammadelta effector cells. A high-resolution transcriptome analysis of all emergent gammadelta thymocyte subsets segregated on the basis of use of the TCR gamma-chain or delta-chain indicated the existence of three separate subtypes of gammadelta effector cells in the thymus. The immature gammadelta subsets were distinguished by unique transcription-factor modules that program effector function.
