Strains of mice with diverse genetic backgrounds were compared for their ability to develop experimental autoimmune dacryoadenitis (EAD) after immunization with a purified lacrimal gland antigen (LG-Ag) in complete Freund’s adjuvant. Susceptibility to the induction of EAD was linked to the murine H-2 histocompatibility background. SJL/J mice with the H-2s haplotype were the most susceptible to EAD, developing extensive cellular infiltration of the lacrimal gland, but those with the H-2d halplotype (BALB/c mice) or H-2q haplotype (DBA/J mice) were resistant to EAD, having little or no infiltration of the lacrimal gland. There was no correlation between the development of EAD and either the antibody response or the in vitro lymphocyte proliferative response to LG-Ag. The differences in the induction of EAD observed between susceptible and resistant strains resided in the different capacity of their lymphocytes to transfer disease. Splenocytes from susceptible SJL/J mice sensitized with LG-Ag in CFA could be activated in vitro with LG-Ag to transfer disease to normal syngeneic recipients. The capacity for adoptive transfer was abrogated by treatment with anti-Thy 1.2 antibody plus complement, an indication that T cells are responsible for the transfer of EAD. However, EAD cannot be transferred with the donor cells from resistant mice even after they have been cultured in vitro with LG-Ag. These results suggest that T cells play a major role in the induction of EAD and that variations in susceptibility are under the control of distinct genetically inherited mechanisms that may include active suppression.
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