| First Author | Chesnutt MS | Year | 1998 |
| Journal | Clin Immunol Immunopathol | Volume | 87 |
| Issue | 1 | Pages | 23-32 |
| PubMed ID | 9576007 | Mgi Jnum | J:47163 |
| Mgi Id | MGI:1202681 | Doi | 10.1006/clin.1997.4492 |
| Citation | Chesnutt MS, et al. (1998) Enhanced lymphoproliferation and diminished autoimmunity in CD4-deficient MRL/lpr mice. Clin Immunol Immunopathol 87(1):23-32 |
| abstractText | MRL/lpr mice spontaneously develop an autoimmune disease with features of systemic lupus erythematosus. They also develop a lymphoproliferative disorder characterized by a massive accumulation of double-negative (DN) T cells that lack both CD4 and CD8. To clarify the role of CD4 in autoimmunity and lymphoproliferation in these mice, CD4-deficient MRL/lpr mice were generated. CD4-deficient MRL/lpr mice developed massive expansion of DN T cells in the blood, spleen, and lymph nodes, which significantly exceeded the degree of lymphoproliferation in CD4-expressing control MRL/lpr mice. Despite this lymphoproliferation, CD4-deficient MRL/lpr mice produced little, if any, antibodies to double-stranded DNA, and they had prolonged survival relative to CD4-expressing littermates. However, they eventually developed moderately severe nephritis, characterized by immunoglobulin and complement deposition in glomeruli, vasculitis, and renal infiltration by CD8+ T cells. These findings indicate that (1) lymphoproliferation in MRL/lpr mice does not require the expression of CD4; (2) autoantibody production in MRL/lpr mice is dependent on the expression of CD4 and not on the accumulation of DN T cells; and (3) the development of nephritis in MRL/lpr mice involves both CD4-dependent and CD4-independent mechanisms. |
