| First Author | Belmonte PJ | Year | 2020 |
| Journal | J Immunol | Volume | 204 |
| Issue | 12 | Pages | 3071-3076 |
| PubMed ID | 32350083 | Mgi Jnum | J:293488 |
| Mgi Id | MGI:6445210 | Doi | 10.4049/jimmunol.2000023 |
| Citation | Belmonte PJ, et al. (2020) Cutting Edge: ST8Sia6-Generated alpha-2,8-Disialic Acids Mitigate Hyperglycemia in Multiple Low-Dose Streptozotocin-Induced Diabetes. J Immunol 204(12):3071-3076 |
| abstractText | The immune system contains a series of checks and balances that maintain tolerance and prevent autoimmunity. Sialic acid-binding Ig-type lectins (Siglecs) are cell surface receptors found on immune cells and inhibit inflammation by recruiting protein tyrosine phosphatases to ITIMs. Islet-resident macrophages express Siglec-E, and Siglec-E expression decreases on islet-resident macrophages as insulitis progresses in the NOD mouse. The sialyltransferase ST8Sia6 generates alpha-2,8-disialic acids that are ligands for Siglec-E in vivo. We hypothesized that engaging Siglec-E through ST8Sia6-generated ligands may inhibit the development of immune-mediated diabetes. Constitutive overexpression of ST8Sia6 in pancreatic beta cells mitigated hyperglycemia in the multiple low-dose streptozotocin model of diabetes, demonstrating that engagement of this immune receptor facilitates tolerance in the setting of inflammation and autoimmune disease. |
