Regulatory effect of the TLR/TACI-MyD88 signaling pathway on immune responses associated with the homing of IgA-producing B cells into salivary glands

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The aim of this basic research project is to clarify the effect of cellular signaling molecule MyD88-mediated immune responses on the homing of IgA-producing B cells into salivary glands, the mechanism of which underlies basic oral immune defense machineries. Through our execution of the experimental plans, it had been figured out that MyD88 deficiency hardly affected IgA production in mouse salivary glands. However, we have found that mouse MyD88 deficiency remarkably suppresses the lymphoid-associated pathogenesis found in female mice, which resembles the pathogenesis of Sjogren's syndrome in humans. Thus, although this study project had not attained our original aim, we have been able to obtain a certain degree of results that are adequate for a basic research project. For our future investigations, we are planning to make efficient use of the results obtained through this project.