| First Author | Singh UP | Year | 2004 |
| Journal | J Leukoc Biol | Volume | 76 |
| Issue | 6 | Pages | 1240-7 |
| PubMed ID | 15356099 | Mgi Jnum | J:94170 |
| Mgi Id | MGI:3511409 | Doi | 10.1189/jlb.0903444 |
| Citation | Singh UP, et al. (2004) Granulocyte chemotactic protein-2 mediates adaptive immunity in part through IL-8R{beta} interactions. J Leukoc Biol 76(6):1240-1247 |
| abstractText | Chemokines constitute a large family of structurally related proteins that play a role in leukocyte migration and differentiation. Indeed, the early expression of human CXC chemokine receptor 1 (hCXCR1) and hCXCR2 [homologous to mouse interleukin (IL)-8Rbeta] ligands by the epithelium is a hallmark of the mucosal host defense. Mice lack IL-8; however, granulocyte chemotactic protein-2 (GCP-2)/lipopolysaccharide-induced CXC chemokine, a murine homologue of human GCP-2, has 32% and 61% sequence identity to human IL-8 and GCP-2, respectively, and binds hCXCR1, hCXCR2, and mouse IL-8Rbeta. To better understand the role of GCP-2 in adaptive immunity and as a nasal adjuvant, we characterized the exogenous effects of this CXC chemokine on cellular and humoral mucosal immune responses. GCP-2 significantly enhanced serum immunoglobulin G (IgG) and mucosal IgA antibodies through increased cytokine secretion by CD4(+) T cells. These alterations in humoral and cellular responses were preceded by an increase in the number of B cells in the nasal tract, a decrease in the number of CD4(+) T cells in the nasal tract as well as cervical lymph nodes, and an increase in the number of neutrophils in the nasal tract 12 h after GCP-2 immunization. This chemokine also modulated CD28 expression by CD4(+) T cells during CD3epsilon stimulation of wild-type mice. GCP-2 increased CD80 and CD86 expression on B cells during in vitro stimulation in a dose-dependent manner. In contrast, cytokine and costimulatory molecule enhancement by GCP-2 was not induced by lymphocytes from IL-8Rbeta(-/-) mice, suggesting that GCP-2 modulates cellular immunity in part through IL-8Rbeta interactions. |
