Histidine Decarboxylase Deficiency Prevents Autoimmune Diabetes in NOD Mice

Figure 2

HDC deficiency increases CD11b⁺Gr-1⁺ and CD11b⁺Ly6G⁺ IMCs. (a) The percentages of CD11b⁺Gr-1⁺ IMCs in BM, spleen, and peripheral blood in wild-type and HDC^−/− mice were measured by FACS analysis (; mean ± s.d. for each group). (b) The relative proportion of CD11b⁺Ly6G⁺ cells in bone marrow, peripheral blood and spleen from wild-type and HDC^−/− mice measured by FACS analysis (; mean ± s.d. for each group). (c) The relative proportion of Ly6G⁺ Ly6C⁻ cells in bone marrow, peripheral blood and spleen of wild-type and HDC^−/− mice measured by FACS analysis (; mean ± s.d. , each group). (d) Bone marrow-derived IMCs from HDC^−/− do not accelerate diabetes onset. Incidence diabetes was measured in NOD RAG^−/− mice after adoptive transfer of pathogenic lymphocytes and CD11b⁺ BM-derived IMCs from wild-type mice or HDC^−/− mice (, compared to indicated control). (e) The percentages of Gr-1⁺CD115⁺ MDSCs in spleen and pancreatic LNs in wild-type and HDC^−/− mice were measured by FACS analysis (; mean ± s.d. for each group). (f) Percentages of CD4⁺CD25⁺ Foxp3⁺ regulatory T cells in spleen and pancreatic LNs in wild-type and HDC^−/− mice were measured by FACS analysis (; mean ± s.d. for each group).

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