Anti-IL2 monoclonal antibody (CABT-48489RM)

Rat Anti-Mouse IL2 monoclonal antibody for ELISA; FC; IP

Additional Formats Available


Host Species
Antibody Isotype
Species Reactivity
Recombinant Mouse IL-2


Application Notes
Flow Cyt: 1/10 - 1/50;
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.


Alternative Names
IL2; interleukin 2; Il-2; interleukin-2; TCGF; T-cell growth factor
Entrez Gene ID
UniProt ID

Product Background

Allograft rejection; Autoimmune thyroid disease; Chagas disease (American trypanosomiasis); Cytokine Signaling in Immune system; Cytokine-cytokine receptor interaction; Cytokines and Inflammatory Response (BioCarta); G beta:gamma signalling through PI3Kgamma; G-protein beta:gamma signalling;


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Custom Antibody Labeling

We offer labeled antibodies using our catalogue antibody products and a broad range of intensely fluorescent dyes and labels including HRP, biotin, ALP, Alexa Fluor® dyes, DyLight® Fluor dyes, R-phycoerythrin (R-PE), at scales from less than 100 μg up to 1 g of IgG antibody. Learn More

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Product Name Cat. No. Applications Host Species Datasheet Price Add to Basket
Rat IgG2b Isotype Control DAGIC1371 FC EIA IHC Rat PDF Inquiry


Influence of inflammasome NLRP3, and IL1B and IL2 gene polymorphisms in periodontitis susceptibility


Authors: de Alencar, Josiane Bazzo; Valentini Zacarias, Joana Maira; Tsuneto, Patricia Yumeko; de Souza, Victor Hugo; de Oliveira e Silva, Cleverson; Laguila Visentainer, Jeane Eliete; Sell, Ana Maria

The pathogenesis of periodontitis (PD) involves several molecules of the immune system that interact in a network to eliminate the periodontopathogens, yet, they contribute to periodontal tissue destruction. The different mechanisms that lead to periodontal tissue damage are not clear. Despite this, immune response genes have been related to the development of PD previously, such as those involved in inflammasomes which are multiprotein complexes and cytokines including Interleukin-1. The aim of the study was to evaluate the polymorphisms in NLRP3 inflammasome, cytokine and receptor of cytokines genes in the development of periodontitis. This case-control study was conducted in 186 patients with PD (stage II and III and grade B) and 208 controls (localized gingivitis and periodontally healthy individuals). Genotyping was performed using PCR-RFLP for the SNP rs4612666 in NLRP3 and using PCR-SSP for IL1A, IL1B, IL1R, IL1RN, IL4RA, INFG, TGFB1, TNF, IL2, IL4, IL6, and IL10. Cytokine serum levels were measured using Luminex technology. SNPStats and OpenEpi software were used to perform statistical analysis. The higher frequencies of NLRP3 T/C and IL1B -511 T/T genotypes and IL2 (+166, -330) GT haplotype were observed in patients with PD compared to controls. The SNPs in NLRP3, IL1R +1970, IL6-174, TNF -308, IL2 +166 and -330, TGFB1 +869 and +915, IL4RA +1902, IL4-1098 and -590 were associated to PD in men. In conclusion, polymorphisms in NLRP3, IL1B and IL2 genes were associated to PD susceptibility. Men carrying the NLRP3, IL1R, IL6, TNF, IL2, TGFB1, IL4RA and IL4 polymorphisms had greater susceptibility than women for developing PD.

Conjunctival Neuropathic and Inflammatory Pain-Related Gene Expression with Contact Lens Wear and Discomfort


Authors: Lopez-de la Rosa, Alberto; Fernandez, Itziar; Garcia-Vazquez, Carmen; Arroyo-del Arroyo, Cristina; Gonzalez-Garcia, Maria J.; Enriquez-de-Salamanca, Amalia

Purpose: To identify alterations in neuropathic and inflammatory pain gene expression associated with contact lens (CL) wear and CL discomfort (CLD). Methods: Eight non-wearers, eight asymptomatic CL wearers (CLWs) and eight symptomatic CLWs were included. Conjunctival cells were collected by impression cytology and the mRNA expression levels of 85 genes were analyzed. Differentially expressed genes between non-wearers and CLWs and between asymptomatic and symptomatic CLWs were analyzed. An enrichment analysis was also performed. Results: Twelve genes were upregulated (including IL10, PDYN and PENK) and 28 downregulated (CCL2, IL1A, IL1B, IL2 and NGF) in CLWs (p <= 0.050). Eleven genes were upregulated (CCL2, IL1A, IL1B, IL2 and NGF) and nine downregulated (PDYN and PENK) in symptomatic CLWs (p <= 0.035). Enriched overrepresented terms were related to pain, neuronal transmission and inflammation. Conclusion: Contact lens wear might produce a desensitization-like mechanism responsible for comfortable CL wear. A malfunction of this mechanism might contribute to CLD.

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