| First Author | Seagal J | Year | 2004 |
| Journal | Immunology | Volume | 112 |
| Issue | 2 | Pages | 265-73 |
| PubMed ID | 15147570 | Mgi Jnum | J:90503 |
| Mgi Id | MGI:3044028 | Doi | 10.1111/j.1365-2567.2004.01883.x |
| Citation | Seagal J, et al. (2004) Contribution of alphabeta and gammadelta T cells to the generation of primary immunoglobulin G-driven autoimmune response in immunoglobulin- mu-deficient/lpr mice. Immunology 112(2):265-73 |
| abstractText | Class switch recombination (CSR) is a T-cell-dependent mechanism regulating isotype switching in activated mature B cells. Recently we showed that T-cell-independent CSRs occur spontaneously during B lymphopoiesis, but such cells are negatively selected by Fas signalling. In immunoglobulin mu-deficient mice, lack of Fas rescues isotype-switched B cells, resulting in generation of an autoimmune primary immunoglobulin G (IgG) repertoire in muMT/lpr mice. In the present study, we studied the role of alphabeta and gammadelta T cells in regulating this primary gammaH-driven repertoire. We found that a lack of alphabeta T cells significantly inhibited IgG production and autoimmunity in muMT/lpr mice, whereas a lack of gammadelta T cells resulted in augmented IgG production and autoimmunity. Also, a lack of T cells in muMT mice rescued isotype-switched B cells and serum IgG, probably owing to the lack of available FasL. We suggest that although CSRs in B-cell lymphopoiesis are T-cell independent, alphabeta T cells are important in the expansion of isotype-switched B-cell precursors and in promoting gammaH-driven autoimmunity, whereas gammadelta T cells regulate these cells. |
