| First Author | Marski M | Year | 2005 |
| Journal | J Immunol | Volume | 175 |
| Issue | 12 | Pages | 7889-97 |
| PubMed ID | 16339524 | Mgi Jnum | J:122246 |
| Mgi Id | MGI:3713627 | Doi | 10.4049/jimmunol.175.12.7889 |
| Citation | Marski M, et al. (2005) CD18 is required for optimal development and function of CD4+CD25+ T regulatory cells. J Immunol 175(12):7889-97 |
| abstractText | CD4+CD25+ T regulatory (Treg) cells inhibit immunopathology and autoimmune disease in vivo. CD4+CD25+ Treg cells' capacity to inhibit conventional T cells in vitro is dependent upon cell-cell contact; however, the cell surface molecules mediating this cell:cell contact have not yet been identified. LFA-1 (CD11a/CD18) is an adhesion molecule that plays an established role in T cell-mediated cell contact and in T cell activation. Although expressed at high levels on murine CD4+CD25+ Treg cells, the role of LFA-1 in these cells has not been defined previously. We hypothesized that LFA-1 may play a role in murine CD4+CD25+ Treg function. To evaluate this, we analyzed LFA-1-deficient (CD18-/-) CD4+CD25+ T cells. We show that CD18-/- mice demonstrate a propensity to autoimmunity. Absence of CD18 led to diminished CD4+CD25+ T cell numbers and affected both thymic and peripheral development of these cells. LFA-1-deficient CD4+CD25+ T cells were deficient in mediating suppression in vitro and in mediating protection from colitis induced by the transfer of CD4+CD25- T cells into lymphopenic hosts. Therefore, we define a crucial role for CD18 in optimal CD4+CD25+ Treg development and function. |
