3 entries found for : it-50
Acovic A, Simovic Markovic B, Gazdic M, Arsenijevic A, Jovicic N, Gajovic N, Jovanovic M, Zdravkovic N, Kanjevac T, Harrell CR, Fellabaum C, Dolicanin Z, Djonov V, Arsenijevic N, Lukic ML, Volarevic V (2018) Indoleamine 2,3-dioxygenase-dependent expansion of T-regulatory cells maintains mucosal healing in ulcerative colitis. Therap Adv Gastroenterol 11:1-22. doi: 10.1177/1756284818793558
Objective: To analyze the significance of the IDO:Treg axis for inducing and maintaining mucosal healing in ulcerative colitis (UC).
Summary: IDO-dependent expansion of endogenous Tregs should be explored as a new approach for induction and maintenance of mucosal healing in patients with UC.
Usage: DSS-treated BALB/c mice were injected with Anti-CD103-SAP (2 mg/kg, intraperitoneally).Related Products: Anti-CD103-SAP (Cat. #IT-50)
Cao Q, Lu J, Li Q, Wang C, Wang X, Lee V, Wang C, Nguyen H, Zheng G, Zhao Y, Alexander S, Wang Y, Harris D (2016) CD103+ dendritic cells elicit CD8+ t cell responses to accelerate kidney injury in adriamycin nephropathy. J Am Soc Nephrol 27:1344-1360. doi: 10.1681/ASN.2015030229
Summary: Although it is known that dendritic cells (DCs) are involved in chronic kidney disease, it is not well understood how they either resolve or aggravate the condition. CD103+ dendritic cells in particular, are known to maintain tolerance through interaction with regulatory T cells, as well as protect against infection through interactions with CD8+ T cells. In this work the authors depleted CD103+ DCs by administering 1 mg/kg of anti-CD103-SAP (Cat. #IT-50) to the intraperitoneal space of mice subject to adriamycin nephropathy. Rat IgG-SAP (Cat. #IT-17) was used as a control. Elimination of the CD103+ DCs attenuated the kidney injury, indicating that in murine chronic kidney disease CD103+ DCs are pathogenic rather than therapeutic.
Zhang L, Hadley GA (2010) Application of anti-CD103 immunotoxin for saving islet allograft in context of transplantation. Chin Med J (Engl) 123(24):3644-51.
Summary: This work investigates whether depletion of CD103-positive cells protects transplanted islets from host-immune cell attack. Diabetes was induced in mice, followed by an islet transplant. Anti-CD103-SAP (Cat. #IT-50) was administered via i.p. injection (1.0 mg/kg or 2.0 mg/kg). Rat IgG-SAP (Cat. #IT-17) was used as a control. Diabetic mice treated with anti-CD103-SAP after islet transplantation had an indefinite survival time as compared to untreated mice that survived fewer than 20 days.