Fig. 4.

Quantitative RT-PCR results (note the different ordinate for each graph). Normalized to β-actin. For all groups of mice, n = 3. (A) Quantitative RT-PCR determined that the mRNA level for CD68 is reduced in mSOD1^G93A/RAG2^−/− mice and restored after mSOD1^G93A BMT. The mSOD1^G93A/CD4^−/− mice also had reduced levels of CD68. These results are consistent with the immunohistochemical observations. (B) The mRNA level for GFAP was increased in all mSOD1^G93A groups of mice. (C–E) There were reduced message levels for IGF-1, GDNF, and BDNF in mSOD1^G93A/RAG2^−/− mice compared with mSOD1^G93A/RAG2^+/− mice at end-stage disease, and the levels were restored after mSOD1^G93A BMT. Message levels for these neurotrophic factors were also reduced in mSOD1^G93A/CD4^−/− mice. Similar results were obtained for GLT-1 (F) and GLAST (G), glutamate transporters predominately localized on astrocytes. (H) IL-4 was reduced in mSOD1^G93A/RAG2^−/− mice compared with mSOD1^G93A/RAG2^+/− mice, but was restored following mSOD1^G93A BMT. mSOD1^G93A/CD4^−/− mice also had a reduced mRNA level for IL-4. (I) TGF-β, an anti-inflammatory/neurotrophic factor, was decreased in mSOD1^G93A/RAG2^−/− mice compared with mSOD1^G93A/RAG2^+/− mice but was again restored following mSOD1^G93A BMT. (J) In contrast to IL-4 and TGF-β, the proinflammatory agent TNF-α was elevated in mSOD1^G93A/RAG2^−/− and mSOD1^G93A/CD4^−/− mice. (K) NOX2, a subunit in the enzyme responsible for the production of highly toxic superoxide molecules, was also elevated in mSOD1^G93A/RAG2^−/− and mSOD1^G93A/CD4^−/− mice. +Increased compared with WT mice, P < 0.05; *, decreased compared with mSOD1^G93A or mSOD1^G93A/RAG2^+/− mice, P < 0.05; ‡, not different from mSOD1^G93A/RAG2^−/− mice; #, not different from mSOD1^G93A/RAG2^+/− mice; **, increased compared with mSOD1^G93A or mSOD1^G93A/RAG2^+/− mice, P < 0.05; ##, decreased compared with mSOD1^G93A/RAG2^−/− mice, P < 0.05.