Rheumatology Advance Access originally published online on February 19, 2007
Rheumatology 2007 46(5):893-894; doi:10.1093/rheumatology/kel441
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Response to Gauster et al.
Department of Pathology, Tennis Court Road, Cambridge CB2 1QP, UK
Correspondence to: E-mail: rla25{at}cam.ac.uk
SIR, We would like to thank Dr Gauster and his colleagues for their interest in our article and their helpful comments regarding the figure on trophoblast MHC-I. In our article, we aimed to assess the relative levels of MHC-I heavy chains compared with conformed MHC-I on the surface of cells from healthy controls and arthritis patients using the monoclonal antibodies HC10 and W6/32. MHC-I heavy chains, as indicated by HC10 reactivity, have been been implicated in the pathogenesis of spondyloarthropathy [1, 2], and we observed an increase in the relative levels of MHC-I heavy chains for arthritic patients compared with healthy controls.
In Figure 4 of our manuscript we used the same antibodies to examine MHC-I heavy chains on trophoblast, as it has been suggested that recognition of FHC on this tissue could contribute to maternal immunoregulation during pregnancy [3]. We again used HC10, in order to allow comparison with results from peripheral blood, and because this antibody had previously been shown to immunoprecipitate both HLA-C and HLA-G [4]. The findings of Gauster and colleagues show that the reactivity of HC10 with HLA-G is not sufficient to stain cells by immunohistochemistry. If a similar situation exists for flow cytometry, it indicates that the particularly high levels of MHC-I heavy chains we observed on trophoblast are, in fact, an underestimate. Thus, in addition to the HLA-G structures previously described [57], we can now conclude that trophoblast HLA-C appears to be present at unusually high levels as heavy chains. If trophoblast MHC-I heavy chain levels are, as Dr Gauster's findings suggest, even higher than our original estimate, it will be important to address their functional relevance. MHC-I heavy chains have been shown to act as a ligand for inhibitory LILR receptors, which are found on maternal decidual macrophages [8, 9], and may therefore suppress maternal macrophage activity. We believe that recognition of MHC-I heavy chains by LILR will prove to be an exciting field in the immunology of pregnancy.
The author has declared no conflicts of interest.
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