Monozygotic twins with distinct forms of idiopathic inflammatory myositis.
نویسندگان
چکیده
HTLV-I carrier showed a relatively small size of ectopic GC whose CXCL13 expression pattern was similar. However, interestingly, the MNCs of HAM–pSS patients demonstrated no expression of CXCL13. In contrast to CXCL13, CXCL12 was commonly expressed on ductal epithelial cells of all the pSS patients irrespective of anti-HTLV-I antibody. In a normal subject, no expression of CXCL13 was observed with positive expression of CXCL12 similar with pSS. The lymphoid aggregates of LSGs are responsible for autoantibody production that locally occurs in ectopic GC [5, 7, 8]. Radiographic destruction of the ductal structure in HTLV-Iseropositive pSS occurs to a lesser extent than in HTLV-Iseronegative pSS, which is a unique characteristic of the former [4]. The chemokines have been found to regulate ectopic GC formation of SS [5]. Xanthou et al. [9] also demonstrated the significance of lymphoid chemokines for lymphoid structure formation in SS, while others have demonstrated an association of CXCL13 expression and ectopic GC formation in SS [7, 8]. Barone et al. [8] found a B cell-dominant expression pattern, whereas the selected expression in acinar and ductal epithelial cells was observed by Salomonsson et al. [7], although the exact roles of these results remain unclear. Our data suggest an important interaction of CXCL13 and ectopic GC in sialadenitis in SS. The tendency towards low levels of radiographic damage in patients with HAM–pSS suggests that salivary-specific cytotoxicity is modified by HTLV-I infection. Due to even expression of CXCL12 irrespective of HTLV-I infection, HTLV-I presumably affects the CXCL13 expression of infected CD4þ T cells. Via inflammatory mediators modulated by HTLV-I tax protein, dysfunction of MNC-lineage cells due to HTLV-I infection is supposed to play an important role.
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ورودعنوان ژورنال:
- Rheumatology
دوره 48 7 شماره
صفحات -
تاریخ انتشار 2009