InVivoMAb anti-mouse Thy1 (CD90)
About InVivoMAb anti-mouse Thy1 (CD90)
The T24/31 monoclonal antibody reacts with mouse Thy1 also known as CD90. Thy1 is a 25-35 kDa GPI-anchored protein belonging to the Ig superfamily that is expressed by thymocytes, peripheral T cells, myoblasts, epidermal cells, and keratinocytes. The function of Thy1 has not been fully elucidated but is thought to play roles in regulation of cell adhesion, apoptosis, metastasis, inflammation, and fibrosis. This antibody is particularly useful for depletion of T lymphocytes.
InVivoMAb anti-mouse Thy1 (CD90) Specifications
Rat IgG2b, κ
|Recommended Isotype Control(s)||InVivoMAb rat IgG2b isotype control, anti-keyhole limpet hemocyanin(BE0090)|
|Recommended InVivoPure Dilution Buffer||InVivoPure pH 7.0 Dilution Buffer(IP0070)|
Mouse Thy-1 protein
in vivo T cell depletion
0.2 μM filtered
Purified from tissue culture supernatant in an animal free facility
Undiluted at room temperature in the dark
InVivoMAb anti-mouse Thy1 (CD90) (Clone: T24/31)Xiong, H., et al. (2016). "Innate Lymphocyte/Ly6C Monocyte Crosstalk Promotes Klebsiella Pneumoniae Clearance." Cell. doi: 10.1016/j.cell.2016.03.017. PubMed
Increasing antibiotic resistance among bacterial pathogens has rendered some infections untreatable with available antibiotics. Klebsiella pneumoniae, a bacterial pathogen that has acquired high-level antibiotic resistance, is a common cause of pulmonary infections. Optimal clearance of K. pneumoniae from the host lung requires TNF and IL-17A. Herein, we demonstrate that inflammatory monocytes are rapidly recruited to the lungs of K. pneumoniae-infected mice and produce TNF, which markedly increases the frequency of IL-17-producing innate lymphoid cells. While pulmonary clearance of K. pneumoniae is preserved in neutrophil-depleted mice, monocyte depletion or TNF deficiency impairs IL-17A-dependent resolution of pneumonia. Monocyte-mediated bacterial uptake and killing is enhanced by ILC production of IL-17A, indicating that innate lymphocytes engage in a positive-feedback loop with monocytes that promotes clearance of pneumonia. Innate immune defense against a highly antibiotic-resistant bacterial pathogen depends on crosstalk between inflammatory monocytes and innate lymphocytes that is mediated by TNF and IL-17A.
Becher, B., et al. (2014). "High-dimensional analysis of the murine myeloid cell system." Nat Immunol 15(12): 1181-1189. PubMed
Advances in cell-fate mapping have revealed the complexity in phenotype, ontogeny and tissue distribution of the mammalian myeloid system. To capture this phenotypic diversity, we developed a 38-antibody panel for mass cytometry and used dimensionality reduction with machine learning-aided cluster analysis to build a composite of murine (mouse) myeloid cells in the steady state across lymphoid and nonlymphoid tissues. In addition to identifying all previously described myeloid populations, higher-order analysis allowed objective delineation of otherwise ambiguous subsets, including monocyte-macrophage intermediates and an array of granulocyte variants. Using mice that cannot sense granulocyte macrophage-colony stimulating factor GM-CSF (Csf2rb(-/-)), which have discrete alterations in myeloid development, we confirmed differences in barrier tissue dendritic cells, lung macrophages and eosinophils. The methodology further identified variations in the monocyte and innate lymphoid cell compartment that were unexpected, which confirmed that this approach is a powerful tool for unambiguous and unbiased characterization of the myeloid system.
Campbell, K. J., et al. (2012). "Elevated Mcl-1 inhibits thymocyte apoptosis and alters thymic selection." Cell Death Differ 19(12): 1962-1971. PubMed
T cells developing in the thymus undergo rigorous positive and negative selection to ensure that those exported to peripheral lymphoid organs bear T-cell receptors (TCRs) capable of reacting with foreign antigens but tolerant of self. At each checkpoint, whether a thymocyte survives or dies is determined by antiapoptotic and proapoptotic Bcl-2 family members. We used Mcl-1 transgenic (tg) mice to investigate the impact of elevated expression of antiapoptotic Mcl-1 on thymocyte apoptosis and selection, making a side-by-side comparison with thymocytes from BCL-2tg mice. Mcl-1 was as effective as Bcl-2 at protecting thymocytes against spontaneous cell death, diverse cytotoxic insults and TCR-CD3 stimulation-driven apoptosis. In three different TCR tg models, Mcl-1 markedly enhanced positive selection of thymocytes, as did Bcl-2. In H-Y TCR tg mice, elevated Mcl-1 and Bcl-2 were equally effective at inhibiting deletion of autoreactive thymocytes. However, in the OT-1tg model where deletion is mediated by a peripheral antigen whose expression is regulated by Aire, Mcl-1 was less effective than Bcl-2. Thus, the capacity of Mcl-1 overexpression to inhibit apoptosis triggered by TCR stimulation apparently depends on the thymocyte subset subject to deletion, presumably due to differences in the profiles of proapoptotic Bcl-2 family members mediating the deletion.
Fischer, M. A., et al. (2011). "CD11b(+), Ly6G(+) cells produce type I interferon and exhibit tissue protective properties following peripheral virus infection." PLoS Pathog 7(11): e1002374. PubMed
The goal of the innate immune system is containment of a pathogen at the site of infection prior to the initiation of an effective adaptive immune response. However, effector mechanisms must be kept in check to combat the pathogen while simultaneously limiting undesirable destruction of tissue resulting from these actions. Here we demonstrate that innate immune effector cells contain a peripheral poxvirus infection, preventing systemic spread of the virus. These innate immune effector cells are comprised primarily of CD11b(+)Ly6C(+)Ly6G(-) monocytes that accumulate initially at the site of infection, and are then supplemented and eventually replaced by CD11b(+)Ly6C(+)Ly6G(+) cells. The phenotype of the CD11b(+)Ly6C(+)Ly6G(+) cells resembles neutrophils, but the infiltration of neutrophils typically occurs prior to, rather than following, accumulation of monocytes. Indeed, it appears that the CD11b(+)Ly6C(+)Ly6G(+) cells that infiltrated the site of VACV infection in the ear are phenotypically distinct from the classical description of both neutrophils and monocyte/macrophages. We found that CD11b(+)Ly6C(+)Ly6G(+) cells produce Type I interferons and large quantities of reactive oxygen species. We also observed that depletion of Ly6G(+) cells results in a dramatic increase in tissue damage at the site of infection. Tissue damage is also increased in the absence of reactive oxygen species, although reactive oxygen species are typically thought to be damaging to tissue rather than protective. These data indicate the existence of a specialized population of CD11b(+)Ly6C(+)Ly6G(+) cells that infiltrates a site of virus infection late and protects the infected tissue from immune-mediated damage via production of reactive oxygen species. Regulation of the action of this population of cells may provide an intervention to prevent innate immune-mediated tissue destruction.