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. Author manuscript; available in PMC: 2018 Apr 19.
Published in final edited form as: Cell Rep. 2018 Jan 30;22(5):1301–1312. doi: 10.1016/j.celrep.2018.01.006

Figure 7. T and B Cell-Deficient Rag1−/− Mice Develop Normal Neuropathic Cold Allodynia, but Not Complete Tactile Allodynia, following SNI Injury.

Figure 7

T cell reintroduction into Rag1−/− mice abolishes tactile sensitivity differences present between Rag1−/− mice and wild-type control littermates (LM) but leaves cold allodynia unaltered.

(A and B) Immunohistochemistry for the monocyte/macrophage marker IBA1 (red) in noninjured (A) and 7-day SNI-injured DRG in Lck Cre-zsGreen mice, which express labeled T cells (green) (B). Scale Bar: 50 µm.

(C) Representative FACS plots of CD4 versus CD8 cell counts from splenic preparation showing cells positive for both markers in the wild-type and in Rag1−/− and T mice, but not Rag1−/− mice (top). Representative FACS plots of CD4 versus B220 counts showing the presence of B cells in wild-type LMs, but not Rag1−/− or reconstituted Rag1−/− mice.

(D) Rag1−/− mice develop less tactile allodynia post-SNI than their LM controls (Rag versus WT, p = 0.003; Rag versus Rag and T, p = 0.002). Reconstituted Rag1−/− mice (Rag1−/− and T) showed full levels of tactile sensitivity (WT versus Rag and T, not significantly different). Significant differences between the values after SNI and their basal measures are shown (**p < 0.01, Rag1−/−mice versus WT littermates [blue #]; Rag1−/− mice versus Rag and T [red #]; #p < 0.05, ##p < 0.01, two-way repeated-measures ANOVA, Bonferroni post hoc test).

(E) Wild-type LMs, Rag1−/−, and T cell-reconstituted mice develop similar neuropathic cold allodynia (no significant differences among the three curves). For (D) and (E), error bars indicate SEM (wild-type LM, n = 15; Rag1−/−, n = 10; Rag1−/− and T, n = 15).