| First Author | González-Tajuelo R | Year | 2017 |
| Journal | Sci Rep | Volume | 7 |
| Pages | 41841 | PubMed ID | 28150814 |
| Mgi Jnum | J:273705 | Mgi Id | MGI:6282786 |
| Doi | 10.1038/srep41841 | Citation | Gonzalez-Tajuelo R, et al. (2017) P-Selectin preserves immune tolerance in mice and is reduced in human cutaneous lupus. Sci Rep 7:41841 |
| abstractText | Mice deficient in P-Selectin presented altered immunity/tolerance balance. We have observed that the absence of P-Selectin promotes splenomegaly with reduced naive T cell population, elevated activated/effector T cell subset, increased germinal center B and Tfh populations and high production of autoreactive antibodies. Moreover, 1.5-3-month-old P-selectin KO mice showed reduced IL-10-producing leukocytes in blood and a slightly reduced Treg population in the skin. With aging and, coinciding with disease severity, there is an increase in the IL17(+) circulating and dermal T cell subpopulations and reduction of dermal Treg. As a consequence, P-Selectin deficient mice developed a progressive autoimmune syndrome showing skin alterations characteristic of lupus prone mice and elevated circulating autoantibodies, including anti-dsDNA. Similar to human SLE, disease pathogenesis was characterized by deposition of immune complexes in the dermoepidermal junction and renal glomeruli, and a complex pattern of autoantibodies. More important, skin biopsies of cutaneous lupus erythematosus patients did not show increased expression of P-Selectin, as described for other inflammatory diseases, and the number of vessels expressing P-Selectin was reduced. |
