Table 1.

Major immune responses under AAT therapy

Disease model	Treatment route	Outcome	Immune cells	Cell-specific outcomes	Ref.
Experimental autoimmune encephalomyelitis (EAE)	Transgenic hAAT	Increased survival, improved disease markers	T cells	Reduced CNS infiltration	5
			Tregs	Expanded in spleen, blood and lymph nodes
Islet transplantation	Exogenous, transgenic hAAT or in-vivo transfection with hAAT plasmid	Improved islet survival, development of tolerance towards islet allografts	Tregs	Expanded in blood and at graft site	6–9
Collagen-induced arthritis (CIA)	Exogenous hAAT or in-vivo transfection with hAAT plasmid	Delayed onset and ameliorated disease development	B cells	Reduced serum levels of autoimmune antibodies	10
Skin transplantation	Exogenous hAAT	Not followed	DC	Turn semi-mature with low CD40 expression, intact inducible CCR7 and intact migration to lymph nodes	8
GVHD	Exogenous AAT	Increased survival	Tregs, T cells	Increased Treg proportion and reduced T effector cells	11
Autoimmune diabetes (NOD mice)	Exogenous hAAT	Increased survival, reduced disease markers	β cells, Tcells	Reduced β cell apoptosis, reduced T cell infiltration to the pancreatic islets	12,13
Crohn's disease (SAMP-1 mice)	Exogenous hAAT	Improved disease markers	T cells, B cells	Reduced inflammation associated colon damage. Reduced lymphocyte infiltration	14
Cancer (B16 melanoma model)	Exogenous hAAT	Intact anti-cancer cell responses	NK cells	Intact NK cell degranulation and cancer cell killing	15
Antigen vaccination	Exogenous or transgenic hAAT	Not followed	B cells	Reduced B cell proliferation and antigen-specific IgG, elevated antigen-specific IgM	16

AAT = α1-anti-trypsin; hAAT = human AAT; NK = natural killer; Ig = immunoglobulin; SAMP-1 = senescence accelerated mouse prone 1; NOD = non-obese diabetic; GVHD = graft-versus-host disease; CNS = central nervous system; T_regs = regulatory T cells.