InVivoMAb anti-mouse LPAM-1 (Integrin α4β7)
Product Details
The DATK32 monoclonal antibody reacts with mouse LPAM-1 also known as integrin alpha 4 beta 7. The 130 kDa integrin β7 chain associates with the 150 kDa integrin α4 (CD49d) chain to form LPAM-1, a member of the Ig superfamily. LPAM-1 is expressed by peripheral lymphocytes, small subsets of thymocytes, and bone marrow progenitors. LPAM-1 binds VCAM-1 (CD106), MAdCAM-1, and fibronectin and facilitates lymphocyte adhesion and migration to the intestine and associated lymphoid tissues. The DATK32 antibody has been reported to block LPAM-1-mediated cell adhesion in vivo.Specifications
| Isotype | Rat IgG2a, κ |
|---|---|
| Recommended Isotype Control(s) | InVivoMAb rat IgG2a isotype control, anti-trinitrophenol |
| Recommended Dilution Buffer | InVivoPure pH 7.0 Dilution Buffer |
| Conjugation | This product is unconjugated. Conjugation is available via our Antibody Conjugation Services. |
| Immunogen | TK1 cells |
| Reported Applications |
in vivo Integrin α4β7 neutralization Flow cytometry |
| Formulation |
PBS, 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 |
| Sterility | 0.2 µm filtration |
| Production | Purified from cell culture supernatant in an animal-free facility |
| Purification | Protein G |
| RRID | AB_1107713 |
| Molecular Weight | 150 kDa |
| Storage | The antibody solution should be stored at the stock concentration at 4°C. Do not freeze. |
Recommended Products
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Recommended Isotype Control(s)
InVivoMAb rat IgG2a isotype control, anti-trinitrophenol
-
Recommended Dilution Buffer
InVivoPure pH 7.0 Dilution Buffer
in vivo Integrin α4β7 neutralization
Duc, D., et al. (2019). "Disrupting Myelin-Specific Th17 Cell Gut Homing Confers Protection in an Adoptive Transfer Experimental Autoimmune Encephalomyelitis" Cell Rep 29(2): 378-390.e374. PubMed
Multiple sclerosis (MS) is a common autoimmune disease of the CNS. Although an association between MS and inflammatory bowel diseases is observed, the link connecting intestinal immune responses and neuroinflammation remains unclear. Here we show that encephalitogenic Th17 cells infiltrate the colonic lamina propria before neurological symptom development in two murine MS models, active and adoptive transfer experimental autoimmune encephalomyelitis (EAE). Specifically targeting Th17 cell intestinal homing by blocking the α4β7-integrin and its ligand MAdCAM-1 pathway impairs T cell migration to the large intestine and dampens EAE severity in the Th17 cell adoptive transfer model. Mechanistically, myelin-specific Th17 cells proliferate in the colon and affect gut microbiota composition. The beneficial effect of blocking the α4β7-integrin and its ligand MAdCAM-1 pathway on EAE is interdependent with gut microbiota. Those results show that disrupting myelin-specific Th17 cell trafficking to the large intestine harnesses neuroinflammation and suggests that the gut environment and microbiota catalyze the encephalitogenic properties of Th17 cells.
in vivo Integrin α4β7 neutralization
Bemark, M., et al. (2016). "Limited clonal relatedness between gut IgA plasma cells and memory B cells after oral immunization" Nat Commun 7: 12698. PubMed
Understanding how memory B cells are induced and relate to long-lived plasma cells is important for vaccine development. Immunity to oral vaccines has been considered short-lived because of a poor ability to develop IgA B-cell memory. Here we demonstrate that long-lived mucosal IgA memory is readily achieved by oral but not systemic immunization in mouse models with NP hapten conjugated with cholera toxin and transfer of B1-8(high)/GFP(+) NP-specific B cells. Unexpectedly, memory B cells are poorly related to long-lived plasma cells and less affinity-matured. They are α4β7-integrin(+)CD73(+)PD-L2(+)CD80(+) and at systemic sites mostly IgM(+), while 80% are IgA(+) in Peyer’s patches. On reactivation, most memory B cells in Peyer’s patches are GL7(-), but expand in germinal centres and acquire higher affinity and more mutations, demonstrating strong clonal selection. CCR9 expression is found only in Peyer’s patches and appears critical for gut homing. Thus, gut mucosal memory possesses unique features not seen after systemic immunization.
in vivo Integrin α4β7 neutralization
Sheridan, B. S., et al. (2014). "Oral infection drives a distinct population of intestinal resident memory CD8(+) T cells with enhanced protective function" Immunity 40(5): 747-757. PubMed
The intestinal mucosa promotes T cell responses that might be beneficial for effective mucosal vaccines. However, intestinal resident memory T (Trm) cell formation and function are poorly understood. We found that oral infection with Listeria monocytogenes induced a robust intestinal CD8 T cell response and blocking effector T cell migration showed that intestinal Trm cells were critical for secondary protection. Intestinal effector CD8 T cells were predominately composed of memory precursor effector cells (MPECs) that rapidly upregulated CD103, which was needed for T cell accumulation in the intestinal epithelium. CD103 expression, rapid MPEC formation, and maintenance in intestinal tissues were dependent on T cell intrinsic transforming growth factor beta signals. Moreover, intestinal Trm cells generated after intranasal or intravenous infection were less robust and phenotypically distinct from Trm cells generated after oral infection, demonstrating the critical contribution of infection route for directing the generation of protective intestinal Trm cells.
in vivo Integrin α4β7 neutralization, Flow Cytometry
Rosser, E. C., et al. (2014). "Regulatory B cells are induced by gut microbiota-driven interleukin-1beta and interleukin-6 production" Nat Med 20(11): 1334-1339. PubMed
Regulatory B cells (Breg cells) differentiate in response to inflammation and subsequently restrain excessive immune responses via the release of interleukin-10 (IL-10). However, the precise inflammatory signals governing their differentiation remain to be elucidated. Here we show that the gut microbiota promotes the differentiation of Breg cells in the spleen as well as in the mesenteric lymph nodes. Perturbation of the gut microbiome imposed either by antibiotic treatment or by changes in the sterility of housing conditions reduces the number and function of Breg cells. Following the induction of arthritis, IL-1beta and IL-6 are produced only in conventionally housed mice and both cytokines directly promote Breg cell differentiation and IL-10 production. Mice lacking IL-6 receptor (IL-6R) or IL-1 receptor 1 (IL-1R1) specifically on B cells have a reduced number of IL-10-producing B cells and develop exacerbated arthritis compared to control animals. Thus, in response to inflammatory signals induced by both the gut flora and arthritis, Breg cells increase in number and restrain excessive inflammation.
in vivo Integrin α4β7 neutralization
Lindebo Holm, T., et al. (2012). "Pharmacological Evaluation of the SCID T Cell Transfer Model of Colitis: As a Model of Crohn’s Disease" Int J Inflam 2012: 412178. PubMed
Animal models are important tools in the development of new drug candidates against the inflammatory bowel diseases (IBDs) Crohn’s disease and ulcerative colitis. In order to increase the translational value of these models, it is important to increase knowledge relating to standard drugs. Using the SCID adoptive transfer colitis model, we have evaluated the effect of currently used IBD drugs and IBD drug candidates, that is, anti-TNF-alpha, TNFR-Fc, anti-IL-12p40, anti-IL-6, CTLA4-Ig, anti-alpha4beta7 integrin, enrofloxacin/metronidazole, and cyclosporine. We found that anti-TNF-alpha, antibiotics, anti-IL-12p40, anti-alpha4beta7 integrin, CTLA4-Ig, and anti-IL-6 effectively prevented onset of colitis, whereas TNFR-Fc and cyclosporine did not. In intervention studies, antibiotics, anti-IL-12p40, and CTLA4-Ig induced remission, whereas the other compounds did not. The data suggest that the adoptive transfer model and the inflammatory bowel diseases have some main inflammatory pathways in common. The finding that some well-established IBD therapeutics do not have any effect in the model highlights important differences between the experimental model and the human disease.