Anti-Mouse MAdCAM-1 (MECA-89) – Purified in vivo PLATINUMTM Functional Grade

Anti-Mouse MAdCAM-1 (MECA-89) – Purified in vivo PLATINUMTM Functional Grade

Product No.: M1421

[product_table name="All Top" skus="M1400"]

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Clone
MECA-89
Target
MADCAM-1
Formats AvailableView All
Product Type
Hybridoma Monoclonal Antibody
Alternate Names
Mucosal addressin cell adhesion molecule-1
Isotype
Rat IgG2a κ
Applications
B
,
FA
,
FC
,
IF
,
IHC
,
IP
,
WB

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Antibody Details

Product Details

Reactive Species
Mouse
Host Species
Rat
Recommended Isotype Controls
Recommended Isotype Controls
Recommended Dilution Buffer
Immunogen
Mouse mesenteric and peripheral lymph node cells
Product Concentration
≥ 5.0 mg/ml
Endotoxin Level
≤ 1.0 EU/mg as determined by the LAL method
Purity
≥95% by SDS Page
≥95% monomer by analytical SEC
Formulation
This monoclonal antibody is aseptically packaged and formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.2 - 7.4 with no carrier protein, potassium, calcium or preservatives added. Due to inherent biochemical properties of antibodies, certain products may be prone to precipitation over time. Precipitation may be removed by aseptic centrifugation and/or filtration.
State of Matter
Liquid
Product Preparation
Functional grade preclinical antibodies are manufactured in an animal free facility using in vitro cell culture techniques and are purified by a multi-step process including the use of protein A or G to assure extremely low levels of endotoxins, leachable protein A or aggregates.
Pathogen Testing
To protect mouse colonies from infection by pathogens and to assure that experimental preclinical data is not affected by such pathogens, all of Leinco’s Purified Functional PLATINUM<sup>TM</sup> antibodies are tested and guaranteed to be negative for all pathogens in the IDEXX IMPACT I Mouse Profile.
Storage and Handling
Functional grade preclinical antibodies may be stored sterile as received at 2-8°C for up to one month. For longer term storage, aseptically aliquot in working volumes without diluting and store at ≤ -70°C. Avoid Repeated Freeze Thaw Cycles.
Regulatory Status
Research Use Only
Country of Origin
USA
Shipping
2 - 8°C Wet Ice
Additional Applications Reported In Literature ?
FA
IHC
IF
IP
WB
FC
B
Each investigator should determine their own optimal working dilution for specific applications. See directions on lot specific datasheets, as information may periodically change.

Description

Description

Specificity
MECA-89 activity is directed against mouse MAdCAM-1.
Background
MAdCAM-1 is a cell adhesion leukocyte receptor expressed by mucosal venules that helps direct lymphocyte traffic into mucosal tissues and regulates the passage and retention of leukocytes1, 2. MAdCAM-1 binds integrin receptor α4β7 and L-selectin2, 3, 4. Two alternatively spliced isoforms of MAdCAM-1 exist5, both of which are capable of binding α4β72.

MECA-89 was generated by immunizing Wistar rats with endothelial cells isolated from BALB/c mesenteric and peripheral lymph nodes 6. Immunohistological screening of hybridomas yielded two mAbs, MECA-367 and MECA-89, that stain high endothelial venules (HEVs) in mucosal lymphoid organs and Peyer’s patches, but not peripheral lymph nodes (axillary, brachial, popliteal, and inguinal). Immunofluorescence staining of high endothelial cells shows that both MECA-367 and MECA-89 react with antigens on the cell surface. The epitopes for MECA-367 and MECA-89 are distinct. MECA-367 recognizes the N-terminal immunoglobulin domain of MAdCAM-l, and MECA-89 recognizes the second immunoglobulin domain 4,5.

MECA-89 reacts with the same vessels as MECA-367 and binds to isolated MECA-367 antigen; however, unlike MECA-367 it has no effect on lymphocyte binding 6. Additionally, MECA-89 has no effect on MAdCAM-1 binding to α4β7 in vitro 7, but L-selectin dependent adhesion is lost in the presence of MECA-89 4. Additionally, MECA-89 has no significant effect on activated cells, but all interactions are inhibited following subsequent injection of anti-α4 Fab fragments 4. In vivo, MECA-89 inhibits L-selectin-dependent rolling but not direct α4β7-dependent attachment of Mn2+ activated lymphocytes.
Antigen Distribution
MAdCAM-1 is a cell surface glycoprotein selectively expressed on high endothelial venules of mucosal lymphoid organs and Peyer’s patches as well as lamina propria venules.
Ligand/Receptor
Integrin a4ß7, CD62L
NCBI Gene Bank ID
UniProt.org
Research Area
Cell Adhesion
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Cell Biology
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Immunology

Leinco Antibody Advisor

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Clone MECA-89 is commonly used in vivo in mice to neutralize or block MAdCAM-1 (Mucosal Addressin Cell Adhesion Molecule-1) function, which plays an essential role in immune cell trafficking, particularly in the context of gut and mucosal immunity. Researchers typically use MECA-89 in mouse models to study mechanisms of leukocyte homing, inflammation, and diseases affecting mucosal tissues.

Key in vivo applications of MECA-89 in mice include:

  • Blocking MAdCAM-1-mediated lymphocyte trafficking: MECA-89 is administered to inhibit the interaction between MAdCAM-1 and its ligands (mainly integrin α4β7), thereby preventing immune cells from migrating into mucosal tissues like the gut and Peyer’s patches.
  • Modeling inflammatory bowel diseases (IBD): By disrupting cell adhesion and trafficking, MECA-89 facilitates the study of pathogenesis, immune responses, and therapeutic targets in models of colitis and other forms of IBD.
  • Examining the role of MAdCAM-1 in diabetes and insulitis: MECA-89 is used in NOD mice (diabetes-prone strain) to investigate the impact of MAdCAM-1 upregulation in peripheral lymph nodes and its involvement in autoimmune diabetes.
  • Studies of mucosal immunity and lymphoid tissue development: By blocking MAdCAM-1, MECA-89 can be used to study lymphocyte homing to mucosal lymphoid tissues, the development of mucosal-associated lymphoid organs, and immune response regulation.
  • Depletion experiments: Used to deplete or neutralize target cells or molecules in vivo to analyze immune processes or inflammatory responses.
  • Supporting techniques: MECA-89 is applied for in vivo labeling, tissue staining, and flow cytometric analysis in live animals and tissue samples, although these are secondary to its functional blocking application.

Summary Table of Common In Vivo Applications of MECA-89 in Mice

ApplicationPurpose
Block/neutralize MAdCAM-1 functionStudy leukocyte homing, mucosal immunity, lymphoid organ development
Model inflammatory bowel diseaseInvestigate gut inflammation mechanisms
Study diabetes/insulitis in NOD miceExamine MAdCAM-1’s role in autoimmune disease
Depletion experimentsRemove/neutralize MAdCAM-1+ cells/molecules
In vivo labeling and tissue stainingVisualize MAdCAM-1 expression in live or excised tissues
Flow cytometry on live tissuesAnalyze cell populations expressing MAdCAM-1

MECA-89 is primarily regarded as a blocking antibody for MAdCAM-1, making it a foundational tool for dissecting immune cell migration and mucosal immune responses in mouse models.

Commonly used antibodies or proteins in combination with MECA-89 (anti-MAdCAM-1) in the literature include integrins (especially α4β7 integrin), other addressins, and standard immune markers such as CD45, B220, and CD40.

Key reagents and markers commonly used alongside MECA-89:

  • α4β7 integrin: MAdCAM-1 is a primary ligand for this integrin, and studies frequently use α4β7 integrin-targeting antibodies to investigate mucosal lymphocyte homing and adhesion.
  • Other addressins and selectin ligands:
    • MECA-367 and MECA-79: MECA-367 is another anti-MAdCAM-1 antibody, and MECA-79 recognizes the peripheral node addressin (PNAd) carbohydrate epitope, used to discriminate between different HEV (high endothelial venule) ligands.
    • CD62L (L-selectin): MAdCAM-1 also interacts with L-selectin, so antibodies against CD62L are sometimes included to study lymphocyte trafficking.
  • Immune cell markers for flow cytometry and tissue immunostaining:
    • CD45 (pan-leukocyte marker)
    • CD40 (B cell activation)
    • B220 (B cell marker)
    • CD23, CD35 (associated with B cells and follicular dendritic cells)

These marker panels are often used in immune tissue studies, notably of mucosal lymphoid organs, Peyer's patches, or lymph node HEVs, to characterize both vascular structure and immune cell populations present in situ.

Summary table:

Antibody/ProteinDescription/Use
α4β7 integrinMain lymphocyte homing receptor for MAdCAM-1; functionally paired
MECA-367Another anti-MAdCAM-1 antibody, different binding domain
MECA-79Binds peripheral node addressin (PNAd), for HEV carbohydrate epitope
CD62L (L-selectin)Lymphocyte homing receptor interacting with MAdCAM-1
CD45Pan-leukocyte marker
B220 (CD45R)B cell marker
CD40, CD23, CD35Additional immune cell/activation markers (B cells, dendritic cells)

These combinations allow delineation of specific endothelial and leukocyte populations, study of lymphocyte homing, and functional differentiation within lymphoid tissues.

Key findings from scientific literature citing clone MECA-89 focus on two distinct research areas, due to ambiguity in the naming: immunological studies with the anti-MAdCAM-1 antibody (clone MECA-89) and studies on the mecA gene in Staphylococcus aureus. However, in antibody and cell biology literature, MECA-89 specifically refers to a rat monoclonal antibody targeting mouse MAdCAM-1, and this is the most likely context for your query.

Key findings from citations of clone MECA-89 (anti-MAdCAM-1 antibody) include:

  • Specificity and Epitope Recognition: MECA-89 recognizes the second immunoglobulin domain of MAdCAM-1, differentiating it from MECA-367, which binds the N-terminal domain.
  • Functional Effects: Unlike MECA-367, MECA-89 does not affect lymphocyte binding to MAdCAM-1 or block MAdCAM-1 binding to the α4β7 integrin in vitro.
  • Impact on Adhesion: MECA-89 inhibits L-selectin-dependent rolling of lymphocytes in vivo, indicating a selective blockade of L-selectin interactions but not direct α4β7-mediated lymphocyte attachment. These findings help dissect the mechanisms of lymphocyte trafficking in mucosal immune responses.
  • Expression Target: MAdCAM-1 is present on high endothelial venules of mucosal lymphoid organs and Peyer’s patches, as well as lamina propria venules, and MECA-89 has been widely used in immunofluorescence for delineating these vascular structures.
  • Research Applications: MECA-89 is valuable in experimental models to study cell adhesion, lymphocyte homing, and the specialized roles of high endothelial venules in mucosal immunity.

Essential context:

  • Distinction from Other Clones: MECA-89 and MECA-367 bind different domains of MAdCAM-1, allowing for functional dissection of MAdCAM-1-mediated processes.
  • Non-Effect on α4β7: MECA-89’s lack of effect on α4β7 binding specifically points to its utility in isolating L-selectin–dependent mechanisms.
  • Tools for Mouse Immunology: As a highly cited reagent, MECA-89 supports a wide range of anatomical and functional studies in mouse mucosal immunology.

Alternative context (less likely but present in search results):

  • Some literature with similar nomenclature to MECA-89 refers to genetic studies on the mecA gene in MRSA; these findings involve the gene’s clonal dissemination, structural organization, and impact on antibiotic resistance, but do not relate to the antibody clone MECA-89.

The most relevant and authoritative findings pertain to the immunological use of clone MECA-89 as an anti-MAdCAM-1 monoclonal antibody in mouse models to study lymphocyte trafficking and mucosal vascular biology.

Dosing Regimens of Clone MECA-89 Across Different Mouse Models

Overview

The dosing regimens for the anti-MAdCAM-1 antibody clone MECA-89 in mouse models are not standardized and are determined primarily by the specific disease context, pharmacokinetic (PK) parameters, and intended pharmacodynamic (PD) effects. However, direct, detailed information on MECA-89 dosing schedules in recent literature is sparse, and regimens appear to be highly model-dependent, reflecting differences in experimental goals and disease models.

Factors Influencing Dosing

  • Disease Context: The primary disease or condition being modeled (e.g., inflammatory bowel disease, lymphocyte trafficking studies) heavily influences the dose and frequency of administration. Different pathologies may require different levels of target engagement or duration of effect.
  • Pharmacokinetics: The PK profile of MECA-89—how the antibody is absorbed, distributed, metabolized, and excreted in mice—will directly affect dosing frequency and amount. For monoclonal antibodies in mice, factors such as target-mediated drug disposition (TMDD), FcRn recycling, and clearance rates are critical.
  • Pharmacodynamics: The desired biological effect (e.g., blockade of lymphocyte homing, modulation of inflammation) also dictates dosing. Some studies may aim for continuous target saturation, while others may test intermittent or pulsed dosing.

Comparison to Related Antibodies

While specific MECA-89 regimens are not detailed in the provided literature, data for related anti-MAdCAM-1 clones (e.g., MECA-367) show that typical administration is via intravenous injection at single doses, but exact amounts and schedules are not specified and likely vary by study. This variability is consistent with the broader trend for therapeutic antibodies in mice, where dosing is tailored to the experimental model and endpoints.

General Principles in Mouse Antibody Dosing

  • Route of Administration: Intravenous injection is common for achieving rapid and complete systemic exposure.
  • Dose Frequency: Depending on the antibody’s half-life and the disease model, dosing may be single or repeated. For antibodies with rapid clearance, multiple doses may be needed to maintain therapeutic levels.
  • Model-Specific Adjustments: As seen with other agents, “humanized” dosing regimens in mice are sometimes designed to match plasma exposure profiles seen in humans, especially when translational relevance is a priority. This approach could theoretically be applied to MECA-89, but there is no evidence in the current literature that this has been done.

Summary Table: Key Determinants of MECA-89 Dosing in Mouse Models

FactorInfluence on DosingExample/Evidence
Disease contextDictates dose level and frequencyModel-dependent
PharmacokineticsAffects clearance, dose intervalAntibody PK in mice
PharmacodynamicsDetermines target engagement neededDesired biological effect
Route of administrationEnsures systemic deliveryIV common
Translational goalsMay guide “humanized” regimensNot reported for MECA-89

Conclusion

Dosing regimens for clone MECA-89 in mouse models are not fixed and must be optimized for each specific experimental context, taking into account disease model, PK/PD characteristics, and the desired biological outcome. There is no universal dosing schedule, and researchers are advised to conduct pilot PK/PD studies to establish appropriate regimens for their particular mouse model and research question.

References & Citations

1. https://www.uniprot.org/uniprotkb/Q61826/entry
2. Schiffer SG, Day E, Latanision SM, et al. Biochem Biophys Res Commun. 216(1):170-176. 1995.
3. Berlin C, Berg EL, Briskin MJ, et al. Cell. 74(1):185-195. 1993.
4. Bargatze RF, Jutila MA, Butcher EC. Immunity. 3(1):99-108. 1995.
5. Briskin MJ, McEvoy LM, Butcher EC. Nature. 363(6428):461-464. 1993.
6. Streeter PR, Berg EL, Rouse BT, et al. Nature. 331(6151):41-46. 1988.
7. Nakache M, Berg EL, Streeter PR, et al. Nature. 337(6203):179-181. 1989.
B
FA
Flow Cytometry
IF
IHC
Immunoprecipitation Protocol
General Western Blot Protocol

Certificate of Analysis

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Formats Available

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Disclaimer AlertProducts are for research use only. Not for use in diagnostic or therapeutic procedures.