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Prepublished online as a Blood First Edition Paper on September 12, 2002; DOI 10.1182/blood-2002-07-2305. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-07-2305v1 101/3/807    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Lillard, J. W. Articles by McGhee, J. R. Search for Related Content PubMed PubMed Citation Articles by Lillard, J. W., Jr Articles by McGhee, J. R. Related Collections Chemokines, Cytokines, and Interleukins Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 February 2003, Vol. 101, No. 3, pp. 807-814 CHEMOKINES MIP-1 and MIP-1 differentially mediate mucosal and systemic adaptive immunity James W. Lillard Jr, Udai P. Singh, Prosper N. Boyaka, Shailesh Singh, Dennis D. Taub, and Jerry R. McGhee From the Department of Microbiology and Immunology, Morehouse School of Medicine, Atlanta, GA; Department of Microbiology and The Immunobiology Vaccine Center, University of Alabama at Birmingham; and Laboratory of Immunology, National Institute on Aging, Gerontology Research Center, Baltimore, MD. Macrophage inflammatory protein-1 (MIP-1) and MIP-1 are distinct but highly homologous CC chemokines produced by a variety of host cells in response to various external stimuli and share affinity for CCR5. To better elucidate the role of these CC chemokines in adaptive immunity, we have characterized the affects of MIP-1 and MIP-1 on cellular and humoral immune responses. MIP-1 stimulated strong antigen (Ag)-specific serum immunoglobulin G (IgG) and IgM responses, while MIP-1 promoted lower IgG and IgM but higher serum IgA and IgE antibody (Ab) responses. MIP-1 elevated Ag-specific IgG1 and IgG2b followed by IgG2a and IgG3 subclass responses, while MIP-1 only stimulated IgG1 and IgG2b subclasses. Correspondingly, MIP-1 produced higher titers of Ag-specific mucosal secretory IgA Ab levels when compared with MIP-1. Splenic T cells from MIP-1- or MIP-1-treated mice displayed higher Ag-specific Th1 (interferon- [IFN-]) as well as selective Th2 (interleukin-5 [IL-5] and IL-6) cytokine responses than did T cells from control groups. Interestingly, mucosally derived T cells from MIP-1-treated mice displayed higher levels of IL-4 and IL-6 compared with MIP-1-treated mice. However, MIP-1 effectively enhanced Ag-specific cell-mediated immune responses. In correlation with their selective effects on humoral and cellular immune responses, these chemokines also differentially attract CD4+ versus CD8+ T cells and modulate CD40, CD80, and CD86 expressed by B220+ cells as well as CD28, 4-1BB, and gp39 expression by CD4+ and CD8+ T cells in a dose-dependent fashion. Taken together, these studies suggest that these CC chemokines differentially enhance mucosal and serum humoral as well as cellular immune responses. © 2003 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: K. Shiraishi, Y. Ishiwata, K. Nakagawa, S. Yokochi, C. Taruki, T. Akuta, K. Ohtomo, K. Matsushima, T. Tamatani, and S. 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