About InVivoMAb anti-mouse CD106 (VCAM-1)
The M/K-2.7 monoclonal antibody reacts with CD106 also known as VCAM-1 and INCAM-110. CD106 is a 110 kDa single chain type I glycoprotein that is expressed primarily on activated vascular endothelial cells but has also been reported on follicular and interfollicular dendritic cells, some macrophages, bone marrow stromal cells, and non-vascular cell populations within joints, kidney, muscle, heart, placenta, and brain. CD106 expression is induced by inflammatory stimuli and cytokines. CD106 binds the integrins CD49d/CD29 (VLA-4) and α4β7 which contribute to leukocyte adhesion, transmigration, and co-stimulation of T cell proliferation.
InVivoMAb anti-mouse CD106 (VCAM-1) Specifications
|Isotype||Rat IgG1, κ|
|Recommended Isotype Control(s)|
|Recommended Dilution Buffer|
|Immunogen||Stromal cells from mouse bone marrow|
|Sterility||0.2 μM filtered|
|Production||Purified from tissue culture supernatant in an animal free facility|
|Molecular Weight||150 kDa|
|Storage||The antibody solution should be stored at the stock concentration at 4°C. Do not freeze.|
InVivoMAb anti-mouse CD106 (VCAM-1) (Clone: M_K-2.7)
Kapitsinou, P. P., et al. (2014). “Endothelial HIF-2 mediates protection and recovery from ischemic kidney injury.” J Clin Invest 124(6): 2396-2409. PubMed
The hypoxia-inducible transcription factors HIF-1 and HIF-2 mediate key cellular adaptions to hypoxia and contribute to renal homeostasis and pathophysiology; however, little is known about the cell type-specific functions of HIF-1 and HIF-2 in response to ischemic kidney injury. Here, we used a genetic approach to specifically dissect the roles of endothelial HIF-1 and HIF-2 in murine models of hypoxic kidney injury induced by ischemia reperfusion or ureteral obstruction. In both models, inactivation of endothelial HIF increased injury-associated renal inflammation and fibrosis. Specifically, inactivation of endothelial HIF-2alpha, but not endothelial HIF-1alpha, resulted in increased expression of renal injury markers and inflammatory cell infiltration in the postischemic kidney, which was reversed by blockade of vascular cell adhesion molecule-1 (VCAM1) and very late antigen-4 (VLA4) using monoclonal antibodies. In contrast, pharmacologic or genetic activation of HIF via HIF prolyl-hydroxylase inhibition protected wild-type animals from ischemic kidney injury and inflammation; however, these same protective effects were not observed in HIF prolyl-hydroxylase inhibitor-treated animals lacking endothelial HIF-2. Taken together, our data indicate that endothelial HIF-2 protects from hypoxia-induced renal damage and represents a potential therapeutic target for renoprotection and prevention of fibrosis following acute ischemic injury.
Brinkman, C. C., et al. (2013). “Peripheral tissue homing receptors enable T cell entry into lymph nodes and affect the anatomical distribution of memory cells.” J Immunol 191(5): 2412-2425. PubMed
Peripheral tissue homing receptors enable T cells to access inflamed nonlymphoid tissues. In this study, we show that two such molecules, E-selectin ligand and alpha4beta1 integrin, enable activated and memory T cells to enter lymph nodes (LN) as well. This affects the quantitative and qualitative distribution of these cells among regional LN beds. CD8 memory T cells in LN that express these molecules were mostly CD62L(lo) and would normally be classified as effector memory cells. However, similar to central memory cells, they expanded upon Ag re-encounter. This led to differences in the magnitude of the recall response that depended on the route of immunization. These novel cells share properties of both central and effector memory cells and reside in LN based on previously undescribed mechanisms of entry.
Chow, A., et al. (2013). “CD169(+) macrophages provide a niche promoting erythropoiesis under homeostasis and stress.” Nat Med 19(4): 429-436. PubMed
A role for macrophages in erythropoiesis was suggested several decades ago when erythroblastic islands in the bone marrow, composed of a central macrophage surrounded by developing erythroblasts, were described. However, the in vivo role of macrophages in erythropoiesis under homeostatic conditions or in disease remains unclear. We found that specific depletion of CD169(+) macrophages markedly reduced the number of erythroblasts in the bone marrow but did not result in overt anemia under homeostatic conditions, probably because of concomitant alterations in red blood cell clearance. However, CD169(+) macrophage depletion significantly impaired erythropoietic recovery from hemolytic anemia, acute blood loss and myeloablation. Furthermore, macrophage depletion normalized the erythroid compartment in a JAK2(V617F)-driven mouse model of polycythemia vera, suggesting that erythropoiesis in polycythemia vera remains under the control of macrophages in the bone marrow and splenic microenvironments. These results indicate that CD169(+) macrophages promote late erythroid maturation and that modulation of the macrophage compartment may be a new strategy to treat erythropoietic disorders.
Thomas, S. Y., et al. (2011). “PLZF induces an intravascular surveillance program mediated by long-lived LFA-1-ICAM-1 interactions.” J Exp Med 208(6): 1179-1188. PubMed
Innate-like NKT cells conspicuously accumulate within the liver microvasculature of healthy mice, crawling on the luminal side of endothelial cells, but their general recirculation pattern and the mechanism of their intravascular behavior have not been elucidated. Using parabiotic mice, we demonstrated that, despite their intravascular location, most liver NKT cells failed to recirculate. Antibody blocking experiments established that they were retained locally through constitutive LFA-1-intercellular adhesion molecule (ICAM) 1 interactions. This unprecedented lifelong intravascular residence could be induced in conventional CD4 T cells by the sole expression of promyelocytic leukemia zinc finger (PLZF), a transcription factor specifically expressed in the NKT lineage. These findings reveal the unique genetic and biochemical pathway that underlies the innate intravascular surveillance program of NKT cells.