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Published ahead of print on March 18, 2005, doi:10.1165/rcmb.2005-0060OC

Am. J. Respir. Cell Mol. Biol., Volume 33, Number 1, July 2005, 48-55

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Submitted on February 10, 2005
Revised on March 16, 2005

Resident Th1-like Effector Memory Cells in Pulmonary Recall Responses to Mycobacterium tuberculosis

Jessica Walrath1, Lynn Zukowski2, Adriana Krywiak2, and Richard F Silver3*

1 Division of Pulmonary and Critical Care Medicine, Case Western Reserve University School of Medicine, Cleveland, OH, USA; Division of Infectious Diseases, Case Western Reserve University School of Medicine, Cleveland, OH, USA, 2 Division of Pulmonary and Critical Care Medicine, Case Western Reserve University School of Medicine, Cleveland, OH, USA, 3 Division of Pulmonary and Critical Care Medicine, Case Western Reserve University School of Medicine, Cleveland, OH, USA; Division of Infectious Diseases, Case Western Reserve University School of Medicine, Cleveland, OH, USA; University Hospitals of Cleveland, and the Louis B. Stokes Cleveland Veterans' Administration Medical Center, Cleveland, OH, USA

* To whom correspondence should be addressed. E-mail: rfs4{at}po.cwru.edu.

We recently described a model of Th1 recall responses based on segmental antigen challenge with purified protein derivative of Mycobacterium tuberculosis (PPD). Bronchoscopic instillation of 0.5 TU of PPD resulted in localized lymphocytic inflammation in PPD-positive subjects only. Recruited lymphocytes were predominantly CD4+ and were enriched for cells capable of PPD-specific IFN{gamma} production. In the current study, we investigated the mechanisms by which this localized recall response is mobilized. Bronchoscopic PPD challenge of skin-test positive subjects resulted in the production of CXCR3 ligands IP-10 and Mig, but not of CCR5 ligands MIP1{alpha} and RANTES, whereas skin-test negative subjects produced none of these chemokines. Baseline BAL cells of skin-test positive subjects produced IP-10 and Mig in response to in vitro stimulation as well. Because IP-10 and Mig are IFN{gamma}-inducible chemokines, these findings suggested that chemokine responses to PPD were facilitated by resident memory cells of the lung. Further studies confirmed that baseline BAL lymphocytes of PPD-positive subjects produce IFN{gamma} in response to PPD, and that, in comparison to peripheral blood, BAL cells are preferentially enriched for PPD-specific lymphocytes. This IFN{gamma} production is predominantly a function of CD4+ T-cells that display the CD45RO+/CCR7- surface phenotype characteristic of effector memory cells.




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