Background: ITP is an acquired autoimmune disease characterized by the production of autoantibodies that mediate platelet destruction. The role of T cells in pathogenesis of ITP is proved by several facts including that antibodies are usually isotype-switched and harbor somatic mutations, consistent with a T cell–dependent response. TIM-3 is a central regulator of T-cell responses. Many studies have demonstrated that a novel immunoregulatory T-cell immunoglobulin and mucin domain containing molecule-3 (TIM-3) influences chronic autoimmune diseases, such as multiple sclerosis. Moreover, association of TIM-3 polymorphisms with susceptibility to several autoimmune diseases has been identified Objectives: The current study aimed to evaluate the possible contribution of TIM-3 polymorphisms in the pathogenesis of ITP and the relation of these polymorphisms to age of disease onset, clinical course of the disease as well as response to different lines of therapy. Material & Methods: The current study evaluated 3 TIM-3 polymorphisms -1516G>T, -574T>G, and 4259G>T in 259 healthy individuals as well as 100 children with ITP. Genotyping was performed by polymerase chain reaction-restriction fragment length polymorphism. Results: Statistical comparisons for the distribution of genotypes and allele frequency for the 3 TIM-3 polymorphisms (“-1516G>T”, “-574T>G” & “4259G>T”) between ITP patients and controls showed no statistically significant difference (p value>0.05). There was a statistically significant association between the -574T>G polymorphism different genotypes (G/G+G/T and T/T) and the age of disease onset in ITP patients (p value = 0.001). Also there was a statistically significant relation between the platelet count at the onset of the disease in the studied ITP patients and TIM-3 “-574T>G” genotypes (p value =0.001).Conclusion: The present study did not detect a relation between the selected TIM-3 SNPs and ITP susceptibility in Egyptian children with ITP. However, we cannot discard a possible association of other variants within the human TIM-3 gene covering region with ITP as a genetic risk factor.