| First Author | Shimizu T | Year | 2004 |
| Journal | Clin Exp Immunol | Volume | 135 |
| Issue | 3 | Pages | 373-9 |
| PubMed ID | 15008968 | Mgi Jnum | J:88576 |
| Mgi Id | MGI:3034152 | Doi | 10.1111/j.1365-2249.2004.02403.x |
| Citation | Shimizu T, et al. (2004) The role of B7 molecules in the cell contact-mediated suppression of T cell mitogenesis by immunosuppressive macrophages induced with mycobacterial infection. Clin Exp Immunol 135(3):373-9 |
| abstractText | We found previously that immunosuppressive macrophages (Mphis) induced by Mycobacterium intracellulare infection (MI-Mphis) transmitted their suppressor signals to target T cells through cell contact with target T cells. In this study, we examined what kinds of Mphi surface molecules are required for such cell-to-cell interaction. First, it was found that a B7-1-like molecule (B7-1LM) recognizable with one of three test clones of anti-B7-1 monoclonal antibodies (mAbs) was required for expression of the Mphi suppressor activity. Neither anti-B7-2, anti-ICAM-1, nor anti-VCAM-1 mAb blocked the Mphi suppressor activity. Second, MI-Mphis increased the expression of B7-1LM in parallel with the acquisition of the suppressor activity. Moreover, MI-Mphis bound with target T cells in a B7-1LM-dependent fashion. Third, mAb blocking of CTLA-4 on target T cells did not reduce the suppressor activity of MI-Mphis, suggesting the role of a putative molecule on target T cells other than CTLA-4 as the receptor for B7-1LM of MI-Mphis. Fourth, concanavalin A (Con A) stimulation of MI-Mphis was needed for effective cell contact with target T cells and subsequent expression of the suppressor activity of MI-Mphis. Fifth, the Con A-induced increase in the suppressor activity of MI-Mphis was inhibited by KN-62 but not by herbimycin A, H-7, nor H-88, indicating that Con A-induced up-regulation of MI-Mphi function is mediated by calmodulin-dependent protein kinase II or ATP/P2Z receptors, but independent of protein tyrosine kinase, protein kinase C, and protein kinase A. These findings indicate that a B7/CTLA-4-independent mechanism is needed for the transmission of the suppressor signals from MI-Mphis to target T cells. |
