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The human form of TIM-1 was initially discovered as a membrane glycoprotein through which the hepatitis A virus can gain entry into a cell. It was also identified as kidney injury molecule 1 (Kim-1), a predicted adhesion molecule that is upregulated on the surfaces of kidney epithelia. It is also expressed on T helper 2 (Th2) cells of the immune system, and following the binding of its natural ligand TIM-4, stimulates T cell expansion and cytokine production in response to viral challenge. It has been suggested that hyperactivation of TIM-1 leads to an increased level of Th2 responsiveness and asthma susceptibility, and antibodies to TIM-1 may therefore be a novel approach to treating asthma.