Collectively, the absence of CD137L induces an immune deviation of CD4+ T cells by polarizing them towards the Th17 phenotype and reduces IL-10-producing CD11b+ cells and hence serum anti-inflammatory IL-10 levels, resulting in more severe lupus-related glomerulonephritis and dermatitis [42,43]. The gene discussed is TNFSF9; the disease is systemic lupus erythematosus.