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The Journal of Immunology, 2003, 171: 6788-6794.
Copyright © 2003 by The American Association of Immunologists

Role of Monocyte Chemotactic Protein-1/CC Chemokine Ligand 2 on {gamma}{delta} T Lymphocyte Trafficking during Inflammation Induced by Lipopolysaccharide or Mycobacterium bovis Bacille Calmette-Guérin 1

Carmen Penido2,*, Adriana Vieira-de-Abreu*, Marcelo T. Bozza{dagger}, Hugo C. Castro-Faria-Neto* and Patrícia T. Bozza3,*

* Laboratório de Imunofarmacologia, Departamento de Fisiologia e Farmacodinâmica, Instituto Oswaldo Cruz, Fundação Oswaldo Cruz, and {dagger} Departamento de Imunologia, Instituto de Microbiologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil

{gamma}{delta} T lymphocytes are involved in a great variety of inflammatory and infectious responses. However, the mechanisms by which {gamma}{delta} T lymphocytes migrate to inflamed sites are poorly understood. In this study we investigate the role of monocyte chemotactic protein (MCP)-1 in regulating {gamma}{delta} T cell migration after LPS or Mycobacterium bovis bacille Calmette-Guérin (BCG) challenge. LPS-induced {gamma}{delta} T cell influx was significantly inhibited by either pretreatment with dexamethasone or vaccinia virus Lister 35-kDa chemokine binding protein, vCKBP, a CC chemokine neutralizing protein, suggesting a role for CC chemokines in this phenomenon. LPS stimulation increased the expression of MCP-1 mRNA and protein at the inflammation site within 6 h. It is noteworthy that LPS was unable to increase MCP-1 production or {gamma}{delta} T cell recruitment in C3H/HeJ, indicative of the involvement of Toll-like receptor 4. {gamma}{delta} T cells express MCP-1 receptor CCR2. Pretreatment with anti-MCP-1 mAb drastically inhibited LPS-induced in vivo {gamma}{delta} T cell mobilization. Indeed, MCP-1 knockout mice were unable to recruit {gamma}{delta} T cells to the pleural cavity after LPS stimulation, effect that could be restored by coadministration of MCP-1. In addition, BCG-induced {gamma}{delta} lymphocyte accumulation was significantly reduced in MCP-1 knockout mice when compared with wild-type mice. In conclusion, our results indicate that LPS-induced {gamma}{delta} T lymphocyte migration is dependent on Toll-like receptor 4 and sensitive to both dexamethasone and CC chemokine-binding protein inhibition. Moreover, by using MCP-1 neutralizing Abs and genetically deficient mice we show that LPS- and BCG-induced {gamma}{delta} T lymphocyte influx to the pleural cavity of mice is mainly orchestrated by the CC chemokine MCP-1.




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