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The saliva flow rate for males, females and males with females (SFR ± SEM, presented as μL/gram/10 min) is shown from 4–28 weeks of age (B6 F, n = 8; B6 M, n = 7; B6.Il17Previous studies have demonstrated that aberrant pathophysiological changes are detected in 4 week old B6.NOD-Aec1Aec2 mice, followed by lymphocytic infiltration at approximately 16–20 weeks of age in male and female B6.NOD-Aec1Aec2 mice, preceded by the loss of secretory function in both sexes mice than the male counterpart during the adaptive phase with progressive severity during the clinical-disease phase.In addition, we have shown that retrograde cannulation of adenovirus serotype 5 (Ad5) vectors expressing IL-17 were able to induce a Sj S-like disease profile, including the appearance of lymphocytic foci, increased cytokine levels, changes in antinuclear antibody profiles, and temporal loss of saliva flow clearly demonstrated that C57BL/6 mice immunized with salivary gland proteins developed overt Sj S symptoms with increased Th17 cells detected in LF of the glands, however, immunized IL-17 knockout (KO) mice lacked Sj S induction.
NOD-Aec1Aec2 mice with sex- and closely age-matched B6 controls to determine the degree of sialadenitis in the glands at the end stage of the disease.
Recent evidence has indicated that estrogen is capable of inducing Th17 cells by activation of its Rorγt transcription factor, however its role in glandular apoptosis, B cell function, and sexual dimorphism has not been examined.
In the present study, we sought to test the hypothesis that Th17 cells are unique antigen-specific T cells responsible for the development of autoantibodies, which target the destruction of the salivary glands and explore whether a sex difference in IL-17 exists in a spontaneous Sj S B6. Our results demonstrate that the elimination of IL-17 restored gland secretory function and reduced sialadenitis more drastically in females.
The recruitment of innate immune cells facilitates an influx of autoantigen-specific B and T cells.
In recent studies, the majority of the antigen-specific T cells are Th17 cells reactive against the type III muscarinic receptor (M3R).