Similarly, in the IBD mouse model, CD11b+Gr-1+ myeloid cells accumulated in the spleens and secondary lymphoid tissues, and only CD11b+Ly6ChiLy6G− MDSCs suppressed the proliferation and production of cytokines by CD4+ T cells, which were mediated by NO, cell-cell contact, and partially by IFN-γ and PGs [48]. The gene discussed is ITGAM; the disease is inflammatory bowel disease.