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* Sir William Dunn School of Pathology, Oxford, United Kingdom; and
The Edward Jenner Institute for Vaccine Research, Compton, Newbury, United Kingdom
Correspondence: Luisa Martinez-Pomares, Sir William Dunn School of Pathology, South Parks Road, Oxford, OX1 3RE, UK. E-mail: Luisa.Martinez-Pomares{at}pathology.ox.ac.uk
The study of the murine macrophage mannose receptor (MR) has been hampered by the lack of specific reagents. We have generated and characterized novel anti-MR monoclonal antibodies and used them to analyze MR expression in primary mouse macrophages (MØ). In BioGel- and thioglycollate-elicited MØ, interleukin (IL)-4 up-regulated total cell-associated MR (cMR), correlating with enhanced surface expression. We investigated the influence of IL-10, a well-characterized deactivator of MØ function, on MR levels and observed that it had a similar effect to IL-4. In both cases, enhanced cMR levels translated into increased production of the soluble form of the receptor (sMR). We have demonstrated the presence of sMR in cultures of stable non-MØ transductants expressing full-length MR, indicating that the proteolytic activity responsible for cMR cleavage is not MØ-restricted. These data support a role for the MR in T helper cell type 2 cytokine-driven, immune responses and suggest a non-MØ contribution to sMR production in vivo.
Key Words: macrophage • shedding
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