Table 1.

T cell immunoglobulin and mucin-domain (TIM)-containing molecules in airway disease

Disease	TIM protein	Function	References
Asthma	TIM-1 (m)	Blocking TIM-1 antibody reduced Th-2-driven allergic response	23
	TIM-1 (m)	Antagonistic TIM-1 antibody increased Th-2-driven allergic response	74
	TIM-1 (m)	Epitope-dependent effect of TIM-1 antibodies on Th-2 response, causing exacerbation or inhibition of airway inflammation	75
	TIM-3 (m)	Blocking antibody administration reduced Th-2-driven allergic response	86
	TIM-1 (m)	Expression increased in T cells	73
	TIM-3 (m)	Expression increased in T cells	87
	TIM-3 (m, h)	Defective apoptotic clearance induces airway hyperresponsiveness. Dependent on TIM-3 polymorphism	88
	TIM-1 (h)	Antagonistic antibody reduced Th-2 response in a humanized asthma mouse model	76
	TIM-2 (m)	TIM-2-deficient mouse demonstrate exacerbated Th-2 response in asthma model	7
	TIM-1/3 (h)	TIM-3 and TIM-1 are not essential for airway hyperresponsiveness	72
Sarcoidosis	TIM-1 (h)	Reduced expression in T cells of non-Löfgren’s patients is in agreement with an exaggerated Th-1 response	77
Sarcoidosis	TIM-3 (h)	Reduced expression in T cell in BAL and blood correlated negatively with CD4/CD8 ratio	77
Tuberculosis	TIM-3 (m/h)	TIM-3 interacted with galectin-9 on macrophages to restrict intracellular bacterial growth	12
Cystic fibrosis	TIM-3 (h)	Constitutive upregulation in bronchial epithelial cells induced IL-8 production	91
Pneumonia	TIM-3 (m)	Galectin-9 intraperitoneal administration reduced IL-17 production and bacterial clearance	89
Pulmonary fibrosis	TIM-1 (m)	Co-stimulation on NKTs enhances the production of IL-4 and inhibits production of IFN-γ	78
Influenza	TIM-3 (m)	Blocking TIM-3–galectin-9 interaction resulted in improved immune response against influenza A virus	90

Abbreviations: BAL, bronchoalveolar lavage; h, human; IFN-γ, interferon-gamma; IL, interleukin; m, mouse; NKTs, natural killer T cells; Th, T-helper.