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Rheumatology 2003; 42: 486-487
© 2003 British Society for Rheumatology
Letters to the Editor |
Microchimerism in Sjögren's syndrome
Cattedra di Reumatologia, Dipartimento di Clinica e Terapia Medica Applicata, Università ‘La Sapienza’, Rome, Italy
SIR, We have read with great interest the article by Endo et al. [1] about a possible contribution of fetal microchimerism to the pathogenesis of Sjögren's syndrome (SS). For the first time, fetal cells were identified in salivary gland tissue obtained from SS patients using both the polymerase chain reaction (PCR) and in situ hybridization. In our previous work [2], we searched for male microchimerism in minor salivary glands obtained from six women with SS and at least one male pregnancy or miscarriage. These women had no other possible causes of microchimerism (transfusion or transplantation). We used the PCR to look for a specific Y-chromosome sequence, SRY, and for the gene homologous to amelogenin in the DNA extracted from the biopsies of minor salivary glands. We did not find any male DNA either in the tissue from women with SS or in the controls. Similarly, Aractingi et al. [3] could not detect male chimeric cells in labial salivary biopsy specimens from patients with SS and a previous male pregnancy, while microchimerism was found in lip salivary gland biopsies from patients with systemic sclerosis and a similar obstetric history, suggesting that the two diseases differ in their pathogenesis.
What can be the reason for the discrepancies between different reports? In our work the mean interval between the male pregnancy and the biopsy was 27 yr (range 21–43), but this interval is not given in the article by Endo et al. It is possible that a shorter lapse of time allows or makes easier the detection of fetal cells in tissues. Moreover, the authors did not specify if the women examined had any other possible source of microchimerism, such as transfusion, which could be responsible for their positive result. Another explanation for the discrepancy between this work and previous studies is the different genetic background of the cases: the persistence of fetal microchimerism seems to be associated with HLA-DQA1*0501 in both the mother and the son [4]. The HLA relationship of host and donor cells contributes to the tolerance of microchimerism and possibly to susceptibility to some autoimmune diseases. In SS the correlation between HLA genotype and microchimerism has not yet been addressed.
Inconclusive evidence about microchimerism and SS has been reported [1–3]. In order to obtain definitive results, it would be necessary to standardize protocols and select adequate case and control populations. The phenomenon of microchimerism needs to be assessed quantitatively, with consideration of genetic factors.
Notes
Correspondence to: F. Carlucci. E-mail: fracarlu{at}tin.it 
References
- Endo Y, Negishi I, Ishikawa O. Possible contribution of microchimerism
to the pathogenesis of Sjögren's syndrome. Rheumatology 2002;41:490–5.
[Abstract/Free Full Text] - Carlucci F, Priori R, Alessandri C, Stoppacciaro A, Valesini G.
Y chromosome microchimerism in Sjögren's syndrome. Ann Rheum Dis 2001;60:1078–9.
[Free Full Text] - Aractingi S, Sibilia J, Meignin V et al. Presence of microchimerism in labial salivary glands in systemic sclerosis but not in Sjogren's syndrome. Arthritis Rheum 2002;46:1039–43.[CrossRef][Web of Science][Medline]
- Lambert NC, Evans PC, Hashizumi TL et al. Cutting edge:
persistent fetal microchimerism in T lymphocytes is associated with HLA-DQA1*0501:
implications in autoimmunity. J Immunol 2000;164:5545–8.
[Abstract/Free Full Text]
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