Figure 3.

The spleen is not necessary in generating autoimmunity. (A) Sham and splenectomized (splx) C57BL/6 wild-type (WT) mice were infected intravenously with 2 × 10⁶ plaque-forming units (PFUs) of lymphocytic choriomeningitis virus strain WE (LCMV-WE). After 1 h, lymphocytic choriomeningitis virus (LCMV) glycoprotein (GP) or nucleoprotein (NP) copies were counted in the liver, spleen, kidney, lung, and iLNs by quantitative real-time polymerase chain reaction (qRT-PCR) (n = 4, from one experiment). Black column = WT sham; white column = WT splx. (B) Sham and splenectomized C57BL/6 mice were intravenously infected with 20 PFU of LCMV-WE. After 6 days, viral titers were measured in the indicated organs (n = 8; pooled from two experiments). Black column = WT sham; white column = WT splx. mLN, mesenteric lymph node; iLNs, inguinal lymph nodes and pLNs, pancreatic lymph nodes. (C,D) Transgenic splenectomized and sham mice expressing the LCMV-GP under control of the rat insulin promoter (RIP-GP mice) were infected with 200 PFU LCMV-WE. (C) Tetramer (Tet) GP33⁺ CD8⁺ T cells in the blood were counted at the indicated time points (n = 8–9, pooled from two experiments). Black squares = RIP-GP sham; white squares = RIP-GP splx. (D) The onset of diabetes was monitored (n = 9–10, pooled from two experiments). Black squares = RIP-GP sham; white squares = RIP-GP splx. Statistical significance was set at the level of P < 0.05 and was determined by two-way analysis of variance (C) and log-rank (Mantel–Cox) test (D). n.s., not significant.