Expression of histocompatibility antigen HLA—DR by salivary gland epithelial cells in Sjögren's syndrome

Fox, Robert I.; Bumol, Thomas F.; Fantozzi, Richard D.; Bone, Robert C.; Schreiber, Robert D.

doi:10.1002/art.1780290908

Cited by 113 publications

(61 citation statements)

References 27 publications

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“…More specifically, stimuli from ductal epithelial cells could also play an important role in lymphomagenesis by the inappropriate activation and retention of B cells within the chronic inflammatory lesions that characterize the condition. Ductal epithelial cells are activated in PSS, expressing elevated levels of HLA-DR [29] and secreting high levels of proinflammatory cytokines [4,30,31]. Comparable data have also been derived from the NOD mouse model of salivary gland inflammation [32].…”

Section: Role Of Epithelial Cellsmentioning

confidence: 99%

Chemokines and Cell Trafficking in Sjögren's Syndrome

Amft

Bowman

2001

Scand J Immunol

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Sjögren's syndrome is a chronic inflammatory condition affecting exocrine glands, manifested clinically as dry eyes and dry mouth. It arises secondary to systemic immune‐mediated diseases such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), scleroderma or ‘primary’ Sjögren's syndrome. Histologically it is characterized by peri‐ductal aggregates of CD4 T lymphocytes, the frequent occurrence of ectopic germinal centres and, in some patients, B‐cell infiltration of ductal epithelium (myoepithelial sialadenitis). This latter lesion is the precursor for the development of low grade (MALT) B‐cell lymphoma. The identification over recent years of chemokines and their receptors enables us to address the specific processes involved in the migration of inflammatory cells into exocrine glands, the development of their secondary structures and patterns of retention within the glands and potentially the subsequent transformation of B cells into mucosa associated lymphoid tissue (MALT) lymphoma.

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Section: Role Of Epithelial Cellsmentioning

confidence: 99%

Chemokines and Cell Trafficking in Sjögren's Syndrome

Amft

Bowman

2001

Scand J Immunol

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“…Malignant lymphomas develop in less than 10% of patients (1). One of the features of the SS salivary gland is an elevated expression of HLA-DR antigens on the salivary epithelial cells (2,3). The HLA-DR molecules are thought to allow epithelial cells to present putative autoantigens to autoreactive T lymphocytes.…”

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confidence: 99%

“…The HLA-DR molecules are thought to allow epithelial cells to present putative autoantigens to autoreactive T lymphocytes. Interferon-␥ (IFN␥) is a major cytokine that is present in the SS salivary gland (4)(5)(6)(7), and it induces HLA-DR expression on salivary epithelial cells (2,7,8). It is believed that mononuclear cell infiltrates containing a predominance of activated T cells develop around the duct in the SS salivary gland as a result of autoimmune reactions between epithelial cells and lymphocytes (9,10).…”

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confidence: 99%

Involvement of the interferon‐γ–induced T cell–attracting chemokines, interferon‐γ–inducible 10‐kd protein (CXCL10) and monokine induced by interferon‐γ (CXCL9), in the salivary gland lesions of patients with Sjögren's syndrome

Ogawa

et al. 2002

Arthritis & Rheumatism

195

147

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Objective. To elucidate the mechanism of the development of T cell infiltrates in the salivary glands of patients with Sjögren's syndrome (SS), we studied T cell-attracting chemokines and their receptors.Methods. The expression of the T cell-attracting chemokines, interferon-␥ (IFN␥)-inducible 10-kd protein (IP-10; also called CXCL10), monokine induced by IFN␥ (Mig; also called CXCL9), and stromal cellderived factor 1 (SDF-1; also called CXCL12), in salivary glands from SS patients was investigated by polymerase chain reaction-enzyme-linked immunosorbent assay (ELISA). Cells that produce chemokines and lymphocytes that express chemokine receptors were identified by immunohistochemistry. The production of IP-10 and Mig proteins by salivary epithelial cells in response to IFN␥ was determined by ELISA.Results. Expression of IP-10 and Mig messenger RNA (mRNA) was significantly up-regulated in SS salivary glands compared with normal salivary glands (both P < 0.01). There was no significant difference in SDF-1 mRNA expression between the SS and normal salivary glands. IP-10 and Mig proteins were predominantly expressed in the ductal epithelium adjacent to lymphoid infiltrates. Most of the CD3؉ infiltrating lymphocytes in dense periductal foci expressed CXCR3, the receptor for IP-10 and Mig. IFN␥ induced the production of high levels of IP-10 and Mig proteins from cultured SS salivary epithelial cells.Conclusion. These findings suggest that IFN␥ stimulates the production of IP-10 and Mig in the SS ductal epithelium, and that IP-10 and Mig are involved in the accumulation of T cell infiltrates in the SS salivary gland. Chemokines or chemokine receptors could be a rational new therapeutic target in SS.

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“…Different factors implied in such reaction were found, such as overexpression of HLA DR molecules (Fox et al, 1986), proinflammatory cytokines (Fox et al, 1998), oncogenes (Skopouli et al, 1992), and autoantigens (Warhen et al, 1998).…”

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confidence: 99%

Big Prolactin 60 kDa is Overexpressed in Salivary Glandular Epithelial Cells from Patients with Sjögren's Syndrome

Steinfeld

Rommes

François

et al. 2000

Laboratory Investigation

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SUMMARY:Characterization of endogenous synthesis of prolactin (PRL) proteins and their cellular localization in labial salivary glands of patients with Sjö gren's syndrome (SS) were achieved. PRL, PRL-receptors (PRL-R), and S100A6 protein were detected by immunohistochemistry. In situ prolactin synthesis was investigated in controls and SS patients by ex vivo incubation of minor salivary glands biopsies and immunoprecipitation assay. Increased PRL-immunoreactivity was found in cytoplasmic acinar epithelial cells in SS patients compared with normal subjects. PRL-R was distributed only in ductal epithelial cells in which S100A6 protein (a PRL-R-associated protein) was also present. PRL, PRL-R, or S100A6-immunoreactivity was not detected in infiltrating mononuclear cells. Immunoprecipitation demonstrated that PRL synthesis occurred in minor salivary glands with increased synthesis of two distinct PRL-like proteins (one major band at 60 kDa and a minor at 16 kDa) in SS glands compared with normal glands. Expression of PRL gene was demonstrated in SS salivary glands using RT-PCR. A positive correlation was found between the presence of PRL-like proteins in acinar epithelial cells of SS patients and clinical extraglandular manifestations. The presence of anti-Ro and anti-La antibodies also positively correlated with a higher percentage of PRL in acinar epithelial cells. In conclusion, PRL-like proteins are synthetized and overexpressed in glandular epithelial cells of labial salivary glands from SS patients and correlate with the aggressiveness of the disease. (Lab Invest 2000, 80:239-247).

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Expression of histocompatibility antigen HLA—DR by salivary gland epithelial cells in Sjögren's syndrome

Cited by 113 publications

References 27 publications

Chemokines and Cell Trafficking in Sjögren's Syndrome

Chemokines and Cell Trafficking in Sjögren's Syndrome

Involvement of the interferon‐γ–induced T cell–attracting chemokines, interferon‐γ–inducible 10‐kd protein (CXCL10) and monokine induced by interferon‐γ (CXCL9), in the salivary gland lesions of patients with Sjögren's syndrome

Big Prolactin 60 kDa is Overexpressed in Salivary Glandular Epithelial Cells from Patients with Sjögren's Syndrome

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