II. The Effects of Thalidomide Treatment on Autoimmune‐Prone NZB and MRL Mice are Consistent with Stimulation of the Central Immune System

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Abstract
We describe here some immunomodulatory effects of thalidomide on autoimmune‐prone mice. The highly increased synthesis of splenic IgM in NZB mice, of splenic and lymph node IgG of different subclasses in MRL/n mice, and of splenic and lymph node IgGl in MRL/lpr mice was markedly inhibited by thalidomide treatment. After a single treatment with 3mg of thalidomide, the following changes were observed in NZB mice: (i) an initial decrease in the numbers of large CD5+μhigh, and in the numbers of total CD5+μ−, CD5−μhigh, CD5+μhigh lymphocyte populations of the pleural cavity followed by a late increase in the numbers of large cells of the three cell populations; (ii) a consistent increase in the numbers of a CD5lowμlow pleural lymphoid population; (iii) a consistent reduction in the numbers of splenic large CD5+ B cells and an oscillatory increase in the number of cells with CD5− phenotype; (iv) a late reduction in the numbers of splenic total CD5+ B cells. These results are consistent with the notion that thalidomide controls a disease‐associated expansion of B cells in autoimmune prone mouse strains through a stimulatory effect of the drug on the immune system.