CD103 / ITGAE Antibody

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FOR RESEARCH USE ONLY! 02/21 CD103 / ITGAE Antibody CATALOG NO.: A2300-50 (50 µg) A2300-100 (100 µg) BACKGROUND DESCRIPTION: ITGAE, also known as CD103, is an integrin that pairs with the beta 7 integrin to form the human mucosal lymphocyte-1 antigen. ITGAE is preferentially expressed in human intestinal intraepithelial lymphocytes (IEL). It has a role in adhesion and may serve as an accessory molecule for IEL activation. ITGAE has been associated with diseases such as hairy cell leukemia and splenic marginal zone lymphoma. The presence of cytotoxic T cells positive for CD103 expression has been linked to prolonged survival in several malignancies, including gastric cancer, and is currently being explored as a prognostic biomarker as well as a potential therapeutic target. ITGAE; Mucosal Lymphocyte 1 Antigen; HML-1 Antigen; Integrin Subunit Alpha E; HUMINAE ALTERNATE NAMES: ANTIBODY TYPE: Rabbit polyclonal HOST/ISOTYPE: Rabbit / IgG IMMUNOGEN: Human CD103 peptide sequence (amino acids 19 to 200) PURIFICATION: Affinity purification MOLECULAR WEIGHT: 130 kDa calculated; 110 kDa observed FORM: Liquid FORMULATION: In PBS with 0.02% sodium azide, 50% glycerol, pH 7.3 SPECIES REACTIVITY: Human, Mouse, Rat STORAGE CONDITIONS: Store at -20 °C. Avoid repeated freeze-thaw cycles APPLICATIONS: Western Blot (WB): 1:500 to 1:2000 dilution This information is only intended as a guide. The optimal dilutions must be determined by the user Western blot analysis of lysates prepared from various cell lines using CD103 antibody RELATED PRODUCTS: Anti-α4β7 Integrin (Vedolizumab), Humanized Antibody (Cat. No. A2140) Anti-Alpha 5 Beta 1 Integrin (Volociximab), Human IgG4 Antibody (Cat. No. A1092) Anti-Integrin Beta-1 Rabbit Monoclonal Antibody (Cat. No. A1598) Anti-Integrin β1 Antibody (Cat. No. A1669) Anti-CD61 / Integrin beta-3 / Platelet Glycoprotein IIIa Antibody (CloneY2/51) (Cat. No. A1556) Anti-Integrin Alpha 4 (Natalizumab), Human IgG4 Antibody (Cat. No. A1444) FOR RESEARCH USE ONLY! Not to be used on humans. 155 S. Milpitas Blvd., Milpitas, CA 95035 USA | T: (408)493-1800 F: (408)493-1801 | www.biovision.com | [email protected] .

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E S BARRIE and others Role of ITGAE in autoimmune 224:3 235–243 Research diabetes Role of ITGAE in the development of autoimmune diabetes in non-obese diabetic mice Elizabeth S Barrie, Mels Lodder, Paul H Weinreb1, Jill Buss, Amer Rajab, Christopher Adin2, Qing-Sheng Mi3 and Gregg A Hadley The Ohio State University Wexner Medical Center, Room 216 Tzagournis Medical Research Facility, Correspondence 420 W 12th Avenue, Columbus, Ohio 43201, USA should be addressed 1Biogen Idec, Cambridge, Massachusetts 02142, USA to G A Hadley 2College of Veterinary Medicine, Columbus, Ohio 43201 USA Email 3Henry Ford Hospital, Detroit, Michigan 48202, USA [email protected] Abstract C There is compelling evidence that autoreactive CD8 Tcells play a central role in precipitating Key Words the development of autoimmune diabetes in non-obese diabetic (NOD) mice, but the " diabetes underlying mechanisms remain unclear. Given that ITGAE (CD103) recognizes an islet- " autoimmune restricted ligand (E-cadherin), we postulated that its expression is required for initiation of " immune system disease. We herein use a mouse model of autoimmune diabetes (NOD/ShiLt mice) to test this " mouse C hypothesis. We demonstrate that ITGAE is expressed by a discrete subset of CD8 T cells that infiltrate pancreatic islets before the development of diabetes. Moreover, we demonstrate that development of diabetes in Itgae-deficient NOD mice is significantly delayed at early Journal of Endocrinology but not late time points, indicating that ITGAE is preferentially involved in early diabetes development. To rule out a potential contribution by closely linked loci to this delay, we treated WT NOD mice beginning at 2 weeks of age through 5 weeks of age with a depleting anti-ITGAE mAb and found a decreased incidence of diabetes following anti-ITGAE mAb treatment compared with mice that received isotype control mAbs or non-depleting mAbs to ITGAE.
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