Human TARC ELISA Kit (DEIA8149)

Regulatory status: For research use only, not for use in diagnostic procedures.

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cell lysates, serum, plasma
Species Reactivity
Intended Use
The Human TARC ELISA Kit is for Detection and Quantification of Human Thymus and Activation-Regulated Chemokine (hTARC) Concentrations in Cell Lysates, Sera and Plasma.
Contents of Kit
1. 96-Well Microplate or Strips Coated w/ Capture Antibody
2. Biotin-Conjugated Detection Antibody
3. Ready-to-Use Avidin-HRP Conjugate Solution
4. Cytokine Protein Standard
5. Ready-to-Use Substrate
6. Stop Solution
7. Adhesive Plate Sealers
8. Wash Buffer (10x)
9. Protein Standard Diluent
10. Detection Antibody Diluent
If used frequently, reagents may be stored at 2-8°C. If used infrequently, reagents should be stored at -20°C. For more detailed information, please download the following document on our website.


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Impaired activation of lesional CD8(+) T-cells is associated with enhanced expression of Programmed Death-1 in Indian Post Kala-azar Dermal Leishmaniasis


Authors: Mukherjee, Shibabrata; Sengupta, Ritika; Mukhopadhyay, Debanjan; Braun, Claudia; Mitra, Sneha; Roy, Susmita; Das, Nilay Kanti; Chatterjee, Uttara; von Stebut-Borschitz, Esther; Chatterjee, Mitali

Post Kala-azar dermal leishmaniasis (PKDL), caused by Leishmania donovani is the dermal sequel of Visceral Leishmaniasis and importantly, is the proposed disease reservoir. The survival of Leishmania parasites within monocytes/macrophages hinges on its ability to effectively nullify immune activation mechanisms. Thus, delineating the disease-promoting immune mechanisms can facilitate development of immunotherapeutic strategies. Accordingly, in the absence of an animal model, this study aimed to delineate the status of CD8(+) T-cells in patients with PKDL. At disease presentation, the absence of CD4(+) T-cells at lesional sites was concomitant with an overwhelming infiltration of CD8(+) T-cells that demonstrated an absence of Perforin, Granzyme and Zap-70, along with an enhanced expression of Programmed Death-1 (PD-1) and the skin-homing CCL17. Additionally, the lesional CCR4(+) CD8(+) population was associated with an enhanced expression of IL-10 and IL-5. In circulation, the enhanced CD8(+) CCR4(+) T-cell population and raised levels of CCL17/22 was associated with an increased frequency of PD-1, while CD127 was decreased. Taken together, in PKDL, the enhanced plasma and lesional CCL17 accounted for the dermal homing of CD8(+) CCR4(+) T-cells, that along with a concomitant upregulation of PD-1 and IL-10 mediated immune inactivation, emphasizing the need for designing immunotherapies capable of reinvigorating T-cell potency.

Randomized phase 1 study of the phosphatidylinositol 3-kinase delta inhibitor idelalisib in patients with allergic rhinitis


Authors: Horak, Friedrich; Puri, Kamal D.; Steiner, Bart H.; Holes, Leanne; Xing, Guan; Zieglmayer, Petra; Zieglmayer, Rene; Lemell, Patrick; Yu, Albert

Background: Phosphatidylinositol 3-kinase p110 delta isoform (PI3K p110 delta) activity is essential for mast cell activation, suggesting that inhibition of PI3K p110 delta might be useful in treating allergic diseases. Objective: We sought to determine the effect of the PI3K p110 delta-selective inhibitor idelalisib on allergic responses. Methods: This phase 1 randomized, double-blind, placebo-controlled, 2 -period crossover study was conducted with the Vienna Challenge Chamber. Grass pollen-induced allergic symptoms were documented during screening. Eligible subjects received idelalisib (100 mg twice daily) or placebo for 7 days, with allergen challenge on day 7. After a 2 -week washout period, subjects received the alternate treatment and repeated allergen challenge. Study measures included safety, nasal and nonnasal symptoms, nasal airflow, nasal secretions, basophil activation, and plasma cytokine levels. Results: Forty-one patients with allergic rhinitis received idelalisib/placebo (n = 21) or placebo/idelalisib (n = 20). Idelalisib treatment was well tolerated. Mean total nasal symptom scores were lower during the combined idelalisib treatment periods compared with placebo (treatment difference [idelalisib - placebo], -1.78; 95% CI, -2.53 to -1.03; P < .001). Statistically significant differences were also observed for the combined treatment periods for total symptom scores, nasal airflow, nasal secretion weight, and nasal congestion scores. The percentage of ex vivo activated basophils (CD63(+)/CCR3(+) cells; after stimulation with grass pollen) was substantially lower for idelalisib-treated compared with placebo-treated subjects. Plasma CCL17 and CCL22 levels were reduced after idelalisib treatment. Conclusion: Idelalisib treatment was well tolerated in patients with allergic rhinitis and appears to reduce allergic responses clinically and immunologically after an environmental allergen challenge.

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