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Prepublished online as a Blood First Edition Paper on September 12, 2002; DOI 10.1182/blood-2002-07-2305.
Submitted August 1, 2002
Accepted September 4, 2002
MIP-1 and MIP-1ß differentially mediate mucosal and systemic Adaptive Immunity
James W Lillard*, Udai P Singh, Prosper N Boyaka, Shailesh Singh, Dennis D Taub, and Jerry R McGhee
Department of Microbiology, Morehouse School of Medicine, Atlanta, GA, USA; Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL, USA
Department of Microbiology, Morehouse School of Medicine, Atlanta, GA, USA
Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL, USA
Laboratory of Immunology, National Institutes of Health, National Institute on Aging, Baltimore, MD, USA
* Corresponding author; email: lillard{at}msm.edu.
Macrophage inflammatory protein - 1 (MIP-1) and MIP-1ß 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-1ß on cellular and humoral immune responses. MIP-1 stimulated strong antigen (Ag)-specific serum IgG and IgM responses, while MIP-1ß 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-1ß only stimulated IgG1 and IgG2b subclasses. Correspondingly, MIP-1ß produced higher titers of Ag-specific mucosal secretory-IgA Ab levels when compared to MIP-1 Splenic T cells from MIP-1- or MIP-1ß- treated mice displayed higher Ag-specific Th1 (IFN- ) as well as selective Th2 (IL-5 and IL-6) cytokine responses than did T cells from control groups. Interestingly, mucosally derived T cells from MIP-1ß-treated mice displayed higher levels of IL-4 and IL-6 compared to 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.
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