Autoimmune diseases have been linked to keloids in observational studies. Yet, the causality underlying this association remains ambiguous. To investigate the causal effects of selected autoimmune diseases, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), type 1 diabetes (T1D), inflammatory bowel disease (IBD), Crohn's disease (CD), and ulcerative colitis (UC), on keloids. We conducted a bidirectional two-sample Mendelian randomization (MR) analysis utilizing publicly released genome-wide association studies summary statistics. The inverse-variance weighted (IVW) method served as the primary analysis tool, supplemented by other methods such as weighted median, weighted mode, and MR Egger regression. Outliers, heterogeneity, and pleiotropy were assessed using the MR-PRESSO outlier test, Cochran's Q test, and MR-Egger regression, respectively. The IVW analysis revealed that genetically determined autoimmune diseases do not causally effect keloids (RA: OR=0.95, 95% CI: 0.89-1.00, p=0.07; SLE: OR=0.98, 95% CI: 0.93-1.02, p=0.34; IBD: OR=1.01, 95% CI: 0.90-1.03, p=0.27; CD: OR=1.02, 95% CI: 0.96-1.09, p=0.56; UC: OR=0.97, 95% CI: 0.90-1.04, p=0.34; T1D: OR=0.98, 95% CI: 0.95-1.01, p=0.27). Reverse IVW MR analysis showed no significant causal effect of keloids on autoimmune diseases. The results from MR-Egger regression, weighted median, and weighted mode methods were consistent with those obtained from the IVW method, and sensitivity analysis suggested that horizontal pleiotropy was unlikely to distort the causal estimates. Our MR analysis does not provide strong evidence supporting causal associations between autoimmune diseases and keloids in the European population.