Disease relevance of sld

• A new animal model for primary Sjögren's syndrome in NFS/sld mutant mice [1].
• These data suggest that in Sjögren's syndrome-like autoimmune dacryoadenitis in NFS/sld mutant mice, the ICAM-1/LFA-1 pathway may play a crucial role in the development and subsequent progression of T-cell-mediated autoimmunity in the lacrimal glands [2].

High impact information on sld

• Friend leukaemia virus-transformed cells, unlike normal stem cells, form spleen colonies in Sl/sld mice [3].
• When we evaluated the age-associated changes in autoimmune exocrinopathy in a NFS/sld murine model for primary Sjögren's syndrome (SS), severe destructive autoimmune lesions developed in the salivary and lacrimal glands in the aged mice, compared with those observed in the younger model [4].
• Significant inflammatory changes develop spontaneously in both the salivary and lacrimal glands of NFS/sld mutant mice thymectomized 3 days after birth without any immunization, whereas no significant inflammatory lesions were found in other organs or in nonthymectomized mice [1].
• RESULTS: After treatment with CyA at 0.1% in the NFS/sld mice, tear function increased, and there was a decrease in lymphocyte infiltration of the LG and a decrease in apoptotic figures among the acinar cells [5].
• PURPOSE: A new animal model, the NFS/sld mutant mouse, was used for primary Sjögren's syndrome to investigate the efficacy of topical and systemic cyclosporin A (CyA) in preventing inflammation of the exocrine glands [6].

Biological context of sld

• The sld mutation is specific for sublingual salivary mucous cells and disrupts apomucin gene expression [7].
• In this study, we report an established and characterized animal model for primary Sjögren's syndrome in NFS/sld mutant mice bearing an autosomal recessive gene with sublingual gland differentiation arrest [1].
• These data provide strong evidence that in autoimmune exocrinopathy resembling SS in NFS/sld mutant mice, the CD86 costimulatory molecule plays a crucial role in the initiation and subsequent progression of Th1-mediated autoimmunity in the salivary and lacrimal glands [8].
• We have analyzed the role of cell adhesion molecules during the development of autoimmune dacryodenitis in an NFS/sld mouse model for primary Sjögren's syndrome [2].

Anatomical context of sld

• NFS/N-sld mice harbor a spontaneous autosomal recessive mutation, sld (sublingual gland differentiation arrest) and histologically display attenuated mucous cell expression in sublingual glands (Hayashi et al. Am J Pathol 132: 187-191, 1988) [7].
• Organ-specific autoimmune exocrinopathy resembling Sjögren's syndrome (SS) that spontaneously develops in NFS/sld mutant mice thymectomized 3 day after birth is dependent on Th1-type CD4+ T cells [9].
• Production of large numbers of hybridomas producing monoclonal antibodies against rat IgE using mast cell-deficient w/wv and sl/sld strains of mice [10].
• Successful production of large numbers of monoclonal antibodies was achieved when mast cell deficient (w/wv and sl/sld) but not conventional (BALB/c, CAF1 or SJL) mice were used [10].
• Intermediate filaments in the cochleas of normal and mutant (w/wv, sl/sld) mice [11].

Other interactions of sld

• Intraperitoneal administration with anti-CD86 (B7.2) MoAb into the murine model for primary SS in NFS/sld mutant mice resulted in dramatically inhibitory effects on the development of autoimmune lesions, while no significant effects were observed when the mice were administered with anti-CD80 (B7.1) MoAb [8].
• When the therapeutic effects of blocking cell adhesion molecules in vivo were examined, antibodies to ICAM-1 in combination with anti-LFA-1 prevented the development of autoimmune lacrimal gland diseases in NFS/sld mice [2].

References