Current
treatments for unwanted antibody responses largely rely
on immunosuppressive drugs compromising overall immunity. New approaches
to achieve antigen-specific tolerance are desirable to avoid unwanted
side effects. Several nanoparticle-based approaches that utilize different
mechanisms to tolerize the B or T cell arms of the humoral immune
response have shown promise for induction of antigen-specific tolerance,
raising the possibility that they could work synergistically if combined.
Earlier we showed that Siglec-engaging tolerance-inducing antigenic
liposomes (STALs) that display both an antigen (Ag) and glycan ligands
of the inhibitory co-receptor CD22 (CD22L) lead to robust antigen-specific
B cell tolerance to protein antigens in naive mice. In another approach,
administration of free Ag with poly(lactic-co-glycolic
acid)–rapamycin nanoparticles (PLGA-R) induced robust antigen-specific
tolerance through production of regulatory T cells. Here we illustrate
that coadministration of STALs together with PLGA-R to naive mice
induced more robust tolerance to multiple antigen challenges than
either nanoparticle alone. Moreover, in K/BxN mice that develop spontaneous
autoimmune arthritis to the self-antigen glucose-6-phosphate-isomerase
(GPI), co-delivery of GPI-LP-CD22L and PLGA-R delayed onset of disease
and in some mice prevented the disease indefinitely. The results show
synergy between B cell-tolerizing STALs and T cell-tolerizing PLGA-R
and the potential to induce tolerance in early stage autoimmune disease.
Sjögren’s syndrome (SS) is a systemic autoimmune disorder affecting approximately 3% of the population in the United States. This disease has a female predilection and affects exocrine glands, including lacrimal and salivary glands. Dry eyes and dry mouths are the most common symptoms due to the loss of salivary and lacrimal gland function. Symptoms become more severe in secondary SS, where SS is present along with other autoimmune diseases like systemic lupus erythematosus, systemic sclerosis, or rheumatoid arthritis. It is known that aberrant activation of immune cells plays an important role in disease progression, however, the mechanism for these pathological changes in the immune system remains largely unknown. This review highlights the role of different immune cells in disease development, therapeutic treatments, and future strategies that are available to target various immune cells to cure the disease.
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