Lymphocyte phenotype and function in pseudolymphoma associated with Sjögren's syndrome.

Fox, Robert I.; Adamson, T. C.; Fong, Sherman; Robinson, Charles Alexander; Morgan, Eric Lease; Robb, James A.; Howell, Francis V.

doi:10.1172/jci110984

Cited by 57 publications

(27 citation statements)

References 37 publications

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“…The specific role of IgA anticardiolipin antibodies in the pathogenesis of Sjogren's syndrome remains unclear. One possible function of the IgA autoantibodies is to help clear cellular debris derived from normal cell turnover, cells destroyed by the immune system, or from potential pathogens within the gland.28 It is likely that IgA anticardiolipin antibodies are made at the salivary gland inflammatory site, as other autoantibodies are produced by lymphocytes eluted from the salivary gland.29 30 As the salivary gland in patients with Sjogren's syndrome is a mucosal site of inflammation, it is likely that local T helper cells facilitate the isotype switch from IgM to IgA antibodies.…”

Section: Discussionmentioning

confidence: 99%

Antiphospholipid antibodies and HLA associations in primary Sjogren's syndrome.

Fei

Staub

et al. 1992

Annals of the Rheumatic Diseases

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Section: Discussionmentioning

confidence: 99%

Antiphospholipid antibodies and HLA associations in primary Sjogren's syndrome.

Fei

Staub

et al. 1992

Annals of the Rheumatic Diseases

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“…These discrepancies may be attributed to several factors, including the relatively small number of patients reported with lymphoma and ascertainment bias in patient referral patterns. However, these differences also may reflect the difficulty in distinguishing lymphoma from extensive infiltrates due to "benign" SS or pseudolymphoma [9]. The lymphomas are predominantly non-Hodgkin's B cell (IgM-K) tumors that arise in the salivary gland and cervical lymph nodes.…”

Section: Development Of Lymphoma In Ssmentioning

confidence: 99%

Reactivation of Epstein-Barr virus in Sjögren's syndrome

Fox

Luppi

Kang

et al. 1991

Springer Semin Immunopathol

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Sjögren's syndrome (SS) is a chronic autoimmune disease characterized by severe dryness of the eyes and mouth, resulting from lymphocytic infiltration of the lacrimal and salivary glands. SS may exist as a primary condition (primary SS, 1.SS) or as a secondary condition (2.SS) in association with rheumatoid arthritis, systemic lupus erythematosus, or progressive systemic sclerosis. In some 1.SS patients, there may be involvement of the extraglandular organs, including skin, kidney, liver, lung and nervous system. Furthermore, these patients may develop a lymphoproliferative syndrome that includes lymphadenopathy and increased risk of lymphoma. In the pathogenesis of SS, a role for Epstein-Barr virus (EBV) has been suggested because: (a) EBV is present in salivary gland epithelial cells of normal individuals and exaggerated immune responses against EBV could play a role in the destruction of salivary glands in SS; (b) SS salivary gland biopsies contain increased levels of EBV DNA in comparison to normal salivary glands, indicating viral reactivation and inability of lymphoid infiltrates to control EBV replication in SS patients; and (c) salivary gland epithelial cells in SS patients express high levels of HLA-DR antigens and may present EBV-associated antigens to immune T cells in SS patients. Therefore, SS may represent a situation in which genetically predisposed individuals (i.e., HLA-DR3-DQA4-DQB2) have a persistent but ineffectual T cell immune response against EBV at its site of latency. Among 14 non-Hodgkin's lymphomas that developed in SS patients, EBV DNA was detected in increased amounts in the tumor tissue of one patient. Characterization of this tumor DNA revealed: (a) polyclonal immunoglobulin gene rearrangements; (b) EBV DNA with an unusual restriction fragment length polymorphism pattern involving the Bam M fragment; and (c) EBV terminal repeat sequences suggestive of viral replication, similar to those reported in EBV lymphomas occurring in other immunocompromised individuals. Early recognition of this clinical problem may allow beneficial use of antiviral agents.

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“…This disorder is particularly well-suited to serve as a model for autoimmune endocrine-exocrine disease, since it is relatively common and the target organs (i.e., salivary glands) are safely accessible to biopsy (9,lO). Studies using monoclonal antibodies and in vitro functional studies have shown that the saliv,ary gland is infiltrated predominantly by T cells of the Leu-3a-positive (OKT4+) subset that have T helperhnducer cell function (10)(11)(12). The salivary glands of these patients are active sites of autoantibody and interleukin-2 (IL-2) production (13,14).…”

Section: Hla-dr By Salivary Gland Epithelial Cells Robert I Fox Thomentioning

confidence: 99%

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

Fox

Bumol

Fantozzi

et al. 1986

Arthritis & Rheumatism

113

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Recent studies have suggested that the induction of HLA—DR antigens on epithelial cells plays an important role in the pathogenesis of autoimmune endocrine‐exocrine disorders. We found that salivary gland epithelial cells (i.e., acinar and ductal cells) in salivary gland biopsy specimens from patients with primary Sjögren's syndrome (keratoconjunctivitis sicca) expressed high levels of HLA—DR antigen, which were detected by staining frozen tissue sections with monoclonal antibodies and immunoperoxidase technique. In contrast, salivary gland epithelial cells from normal subjects did not express this antigen. Lymphocytes eluted from the salivary gland biopsy specimens of patients who had Sjögren's syndrome produced a soluble factor that stimulated HLA—DR synthesis by a salivary gland‐derived cell line (Sal‐1). These tissue culture supernatants contained γ‐interferon, and their ability to induce HLA—DR synthesis was blocked by monoclonal anti‐γ‐interferon antibody. These results demonstrate the presence of HLA—DR antigen on salivary gland epithelial cells and suggest that local production of γ‐interferon plays a role in this induction.

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Lymphocyte phenotype and function in pseudolymphoma associated with Sjögren's syndrome.

Cited by 57 publications

References 37 publications

Antiphospholipid antibodies and HLA associations in primary Sjogren's syndrome.

Antiphospholipid antibodies and HLA associations in primary Sjogren's syndrome.

Reactivation of Epstein-Barr virus in Sjögren's syndrome

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

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