Disease relevance of Timd2

• Administration of Tim-2 Ig during the induction phase reduces the severity of experimental autoimmune encephalomyelitis, a Th1-mediated autoimmune disease model of multiple sclerosis [1].
• In this study, we report the phenotype of the TIM-2 gene-deficient mouse, and demonstrate exacerbated lung inflammation in an airway atopic response model [2].

High impact information on Timd2

• Class IV semaphorin Sema4A enhances T-cell activation and interacts with Tim-2 [3].
• In addition, expression cloning shows that the Sema4A receptor is Tim-2, a member of the family of T-cell immunoglobulin domain and mucin domain (Tim) proteins that is expressed on activated T cells [3].
• TIM-2 is expressed on B cells and in liver and kidney and is a receptor for H-ferritin endocytosis [4].
• TIM-2 also is expressed in the liver, especially in bile duct epithelial cells, and in renal tubule cells [4].
• We demonstrate that mouse TIM-2 is expressed on all splenic B cells, with increased levels on germinal center B cells [4].

Biological context of Timd2

• Tim-2 regulates T helper type 2 responses and autoimmunity [1].

Anatomical context of Timd2

• We further demonstrate that TIM-2 is a receptor for H-ferritin, but not for L-ferritin, and expression of TIM-2 permits the cellular uptake of H-ferritin into endosomes [4].

Other interactions of Timd2

• We propose that Tim-2, an orthologue of human Tim-1, is critical for the regulation of Th2 responses during autoimmune inflammation [1].

Analytical, diagnostic and therapeutic context of Timd2

• Immune responses in the TIM-2-deficient mouse reveal disregulated expression of Th2 cytokines, and adoptive transfer experiments show that the T cell compartment is responsible for the heightened inflammatory phenotype [2].

References