Clues to pathogenesis

What triggers the production of cold agglutinins? Why are they monoclonal? The precise details are not yet known. The transient cold agglutinin syndrome that follows M. pneumoniae infection offers a unique opportunity to study aspects of the mechanism of stimulation of anti-I production. Negligible amounts of I antigen can be detected on cultured M. pneumoniae, and there is evidence that this represents passively adsorbed material, probably in association with other lipids and glycolipids, from the serum. As autoantibodies to other glycolipids in the serum, e.g. those with blood group A, B, H, and Lewis activities, do not prevail in this infection, it is unlikely that the anti-I are directed against this passively adsorbed form of the I antigen. On the other hand, the receptors on host cells to which the mycoplasma adheres are sialo-oligosaccharide sequences such as structures 7 and 9, that are based on backbones of Ii type, the highest affinity binding being to the branched I type, structure 9. It seems likely that the selective production of high titer anti-I (i.e. 'antireceptor' antibodies) following M. pneumoniae infection is somehow related to these interactions. Possibly the lipid rich mycoplasma serves as an adjuvant overcoming tolerance to self-antigen I. It should be noted that the sialo oligosaccharide receptor sequences occur not only on erythrocytes but also on B and T lymphocytes as well as monocytes, for example. Thus there remains considerable scope for dissection of the macromolecular interactions that culminate in the production of auto-anti-I.

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