"Lymphoid" chemokine messenger RNA expression by epithelial cells in the chronic inflammatory lesion of the salivary glands of Sjogren's syndrome patients - Possible participation in lymphoid structure formation

Citation
G. Xanthou et al., "Lymphoid" chemokine messenger RNA expression by epithelial cells in the chronic inflammatory lesion of the salivary glands of Sjogren's syndrome patients - Possible participation in lymphoid structure formation, ARTH RHEUM, 44(2), 2001, pp. 408-418
Citations number
42
Categorie Soggetti
Rheumatology,"da verificare
Journal title
ARTHRITIS AND RHEUMATISM
ISSN journal
00043591 → ACNP
Volume
44
Issue
2
Year of publication
2001
Pages
408 - 418
Database
ISI
SICI code
0004-3591(200102)44:2<408:"CMREB>2.0.ZU;2-6
Abstract
Objective. Many studies have shown that the microanatomic organization of i nfiltrating leukocytes in the salivary gland lesions of patients with Sjogr en's syndrome (SS) resembles the structure of lymphoid organs. A newly defi ned set of chemokines referred to as "lymphoid," which orchestrate leukocyt e microenvironmental homing and contribute to the formation of lymphoid str uctures, provides directional clues. The aim of this study was to investiga te the possible existence of "lymphoid" chemokines in the chronic inflammat ory lesions of SS patients and thus validate their potential involvement in the disease process. Methods. Twelve patients with primary SS, 3 patients with secondary SS, 4 p atients with other autoimmune disorders, and 4 control individuals were the subjects of this study. Reverse transcriptase-polymerase chain reaction an alysis was performed in order to examine the messenger RNA (mRNA) expressio n of "lymphoid" chemokines. Furthermore, in situ hybridization studies reve aled chemokine mRNA localization. Immunohistochemistry was also applied in order to identify the cell types that expressed the chemokine mRNA. Results. STCP-1/monocyte-derived chemokine and TARC mRNA were expressed in the majority of patients with primary and secondary SS, in 2 of 4 patients with other autoimmune disorders, and in 2 of 4 controls. BCA-1, ELC, and PA RC mRNA were only detected in patients with primary and secondary SS. SLC m RNA was also detected in I non-SS patient. The main cellular sources of che mokine mRNA were ductal epithelial cells and infiltrating mononuclear leuko cytes. Conclusion. The expression pattern of "lymphoid" chemokine mRNA points furt her to the role of epithelial cells in the pathogenesis of SS and offers ne w insight into the potential mechanisms that could be involved in leukocyte attraction and in the in situ formation of secondary lymphoid tissue struc tures.