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1 From the Departments of Ophthalmology and 2 Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland; and the 4 Departments of Immunology and Microbiology and 5 Medicine, Wayne State University School of Medicine, Detroit, Michigan.
PURPOSE. MRL/MpJ-+/+ (MRL/+) and MRL/MpJ-lpr/lpr (MRL/lpr) mice show spontaneous development of a T-cell–driven lacrimal gland inflammation that is a model for Sjögren syndrome. The lacrimal gland lesions in these mice were evaluated by quantitative RT-PCR for selected cytokine mRNA for the relative contributions of T-helper (Th)1 versus Th2 immune responses and by RT-PCR and immunohistochemistry for the contribution of the interleukin (IL)-2/IL-2 receptor (IL-2R) autocrine pathway.
METHODS. RNA was isolated from lacrimal glands of MRL/+ mice ages 1 to 9 months
and from MRL/lpr mice ages 1 through 5 months, and competitive RT-PCR
was used to quantify mRNA for the cytokines IL-2, -4, -10, and -12 and
interferon (IFN)-
. Frozen sections of lacrimal glands from MRL/+ and
MRL/lpr mice ages 2 through 5 months were stained for the IL-2R.
RESULTS. IL-2 and -12 mRNA transcripts were below the limit of detection
(<10-3 fg/pg hypoxanthine phosphoribosyl transferase
gene; HPRT) in both MRL/+ and MRL/lpr mice of all ages.
When detectable, IFN- transcripts were present in low amounts and
were below the limit of detection in most samples. IL-4 transcripts
were present in 100- to 1000-fold greater amounts than IFN-
transcripts. IL-10 transcripts were detectable in both MRL/+ and
MRL/lpr mice. IL-2R typically was detected on less than 10% of
lymphocytes infiltrating lacrimal gland lesions in both substrains.
CONCLUSIONS. On the basis of RT-PCR for cytokine mRNA, autoimmune lacrimal gland lesions in MRL/+ and MRL/lpr mice appear to be largely Th2-mediated. There does not appear to be a direct role for the IL-2/IL-2R autocrine pathway within the microenvironment of the lacrimal gland.
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