Abstract
Although anti-C1q autoantibodies have been described more than four decades ago a constant stream of papers describing clinical associations or functional consequences highlights that anti-C1q antibodies are still hot and happening. By far the largest set of studies focus on anti-C1q antibodies is systemic lupus erythematosus (SLE). In SLE anti-C1q antibodies associate with involvement of lupus nephritis in such a way that in the absence of anti-C1q antibodies it is unlikely that a flare in nephritis will occur. Anti-C1q antibodies occur in several autoimmune conditions but also in healthy individuals. Although considerable progress has been made in the understanding of how anti-C1q antibodies may contribute to tissue injury there is still a lot to learn about the processes involved in the breaking of tolerance to this protein. There has been considerable improvement in the assays employed to test for the presence of anti-C1q antibodies. Hopefully with these new and standardized assays at hand larger clinical association studies will be conducted with independent replication. Such large-scale studies will reveal the true value of clinical testing for anti-C1q autoantibodies in several clinical conditions.
Highlights
Of all the autoantibodies that target complement proteins, antiC1q autoantibodies have received most attention (Trouw et al, 2001; Norsworthy and Davies, 2003)
C1q does so only when at least two IgG molecules are spatially oriented in such a way that they can simultaneously interact with one C1q molecule as for example in an immune-complex (Cooper, 1985)
In the following years these low-molecular weight fractions were further identified as monomeric, non-complexed IgG molecules that interacted with the collagen-like tail of the C1q molecule (Uwatoko et al, 1984, 1987; Antes et al, 1988)
Summary
Of all the autoantibodies that target complement proteins, antiC1q autoantibodies have received most attention (Trouw et al, 2001; Norsworthy and Davies, 2003). The blessing lies in the fact that the identification of antiC1q antibodies was a consequence of studies on size fractionations of immune complexes that could bind to C1q.
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