The changes of myoepithelial cells of sialoadenitis in submandibular glands in lupus-prone female NZB x NZWF1 (B/WF1) mice, a model for human secondary Sjögren's syndrome (sSS), were examined ultrastructurally. Inflammatory foci consisting of mainly lymphoid cells (lymphocytes and plasma cells) in the interlobular interstitium began to develop from 18 weeks of ages, and those were found within acini from the age of 25 weeks. These were paralleled with the production of anti-double-stranded deoxyribonucleic acid and anti-Ro/SS-A antibodies with age. Infiltrated lymphoid cells consisted of CD4+ T cells and Ig+ (or IgG2a+) cells. Electron microscopy revealed destruction of myoepithelial cells with lysis of basement membranes contacted with either lymphocytes or plasma cells. These led to the destruction (degeneration and necrosis) of the epithelium in striated and intercalated ducts and acinar epithelium. Further destruction of those cells occurred by the invasion of lymphocytes into the epithelial layers. Small numbers of apoptotic myoepithelium and duct epithelium from the age of 25 to 36 weeks and an increase of those cells in survived mice at 44 weeks of age were observed. The present study suggests that the myoepithelium may be one of the target cells and that the destruction of myoepithelial cells by infiltrated lymphoid cells may precede the destruction of acinar ducts and epithelium in sialoadenitis in sSS.
Summary
The mechanisms of distant manifestation after a local allergic reaction are largely unknown. This study examined the development of cutaneous lesions in a mouse model of late allergic rhinitis (LAR). BALB/c mice were sensitized by ovalbumin (OVA) intraperitoneally two times (on days 0 and 10) and challenged by OVA intranasally on day 14. Four days after OVA challenge, nasal and cutaneous lesions including helper T (Th) responses, expression of adhesion molecules and presence of OVA and IgE were examined, and compared with unsensitized and unchallenged (control) mice. Compared with the control group, the LAR group developed LAR characterized by infiltration of lymphocytes and eosinophils, increased IgE values and increased productions of IL‐4 and IL‐5, but not IFN‐γ. A dominant infiltration of eosinophils and increase in mast cells, attachment of eosinophils to endothelium, intense expression of VCAM‐1 on endothelium in venules and VLA‐4 expression on eosinophils and mast cells were recognized in the cutaneous tissues. There were no differences in the expression of ICAM‐1 on vascular endothelium and LFA‐1 on infiltrated leucocytes between the two groups. CLA expression on lymphocytes was not detected, and the binding of OVA and IgE on mast cells and eosinophils was found in the cutaneous lesions in the LAR group, but not in the control group. This study suggests that acute uriticaria‐like lesions in OVA‐unexposed cutaneous tissues may be induced by immediate allergic reaction due to the systemic development of Th2‐type response in a mouse model of LAR.
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