| First Author | Deng GM | Year | 2013 |
| Journal | J Immunol | Volume | 191 |
| Issue | 7 | Pages | 3563-7 |
| PubMed ID | 23980209 | Mgi Jnum | J:205963 |
| Mgi Id | MGI:5547475 | Doi | 10.4049/jimmunol.1300634 |
| Citation | Deng GM, et al. (2013) T cell CD3zeta deficiency enables multiorgan tissue inflammation. J Immunol 191(7):3563-7 |
| abstractText | Although a population of T cells with CD3zeta chain deficiency has been found in patients with systemic lupus erythematosus, rheumatoid arthritis, cancer, and infectious disease, the role of CD3zeta chain in the disease pathogenesis remains unknown. To understand the contribution of CD3zeta deficiency to the expression of organ injury, we have performed the following studies. We used CD3zeta-deficient mice to investigate the role of CD3zeta in the pathogenesis of organ tissue inflammation. We found that the CD3zeta(-/-) mice can spontaneously develop significant organ inflammation that can be accelerated following the administration of polyinosinic:polycytidylic acid or allogeneic cells (graft versus host). T cells from CD3zeta(-/-) mice display increased expression of the adhesion molecules CD44 and CCR2 and produce increased amounts of IFN-gamma blockade, which mitigates tissue inflammation. Our results demonstrate that CD3zeta deficiency bestows T cells with the ability to infiltrate various tissues and instigate inflammation. Decreased CD3zeta expression noted in T cells from various diseases contributes independently to tissue inflammation and organ damage. Approaches to restore CD3zeta expression of the surface of T cells should be expected to mitigate tissue inflammation. |
