Tim-1 regulates Th2 responses in an airway hypersensitivity model

Miranda L. Curtiss, Jacob V. Gorman, Thomas R. Businga, Geri Traver, Melody Singh, David K. Meyerholz, Joel N. Kline, Andrew J. Murphy, David M. Valenzuela, John D. Colgan, Paul B. Rothman, Suzanne L. Cassel

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


T-cell immunoglobulin mucin-1 (Tim-1) is a transmembrane protein postulated to be a key regulator of Th2-type immune responses. This hypothesis is based in part upon genetic studies associating Tim-1 polymorphisms in mice with a bias toward airway hyperrespon-siveness (AHR) and the development of Th2-type CD4 + T cells. Tim-1 expressed by Th2 CD4 + T cells has been proposed to function as a co-stimulatory molecule. Tim-1 is also expressed by B cells, macrophages, and dendritic cells, but its role in responses by these cell types has not been firmly established. Here, we generated Tim-1-deficient mice to determine the role of Tim-1 in a murine model of allergic airway disease that depends on the development and function of Th2 effector cells and results in the generation of AHR. We found antigen-driven recruitment of inflammatory cells into airways is increased in Tim-1-deficient mice relative to WT mice. In addition, we observed increased antigen-specific cytokine production by splenocytes from antigen-sensitized Tim-1-deficient mice relative to those from controls. These data support the conclusion that Tim-1 functions in pathways that suppress recruitment of inflammatory cells into the airways and the generation or activity of CD4 + T cells.

Original languageEnglish (US)
Pages (from-to)651-661
Number of pages11
JournalEuropean Journal of Immunology
Issue number3
StatePublished - Mar 2012
Externally publishedYes


  • Allergy
  • Asthma
  • Th2
  • Tim-1

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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