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Our findings demonstrate that agonist peptides can be used in immunization protocols for breaking of tolerance and induction of CTL that mediate effective anti-tumor responses.
That all anti-HIV MAbs, including the bNt MAbs, share similar features indicates that unusual immunological processes, such as breaking of tolerance [19], are probably not responsible for the rarity of the bNt Abs during chronic HIV infection.
IFN-α can contribute to the breaking of tolerance and to the induction/expansion of auto-reactive T and B cells through direct effects on these cells or by modulating immune functions through the induction of DC costimulatory molecules and soluble factors [1], [4].
Such immune activation might contribute to breaking of tolerance to autoantigens, leading to the induction of autoimmune disease [ 16].
This result suggests that the breaking of tolerance to self requires more than a simple exposure to NETs.
Individuals deficient in C1 components, C2 and C4, have a high prevalence of lupus due to impaired clearance of ICs/apoptotic bodies leading to breaking of tolerance.
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SLE represents a prototypic autoimmune disease characterized by a break of tolerance to self molecules, for which the possible pathogenetic role of IFN-α has been strongly emphasized [3].
The mechanism by which PADI4 variability may influence the break of tolerance is still unknown.
Are antibodies induced by the break of tolerance able to inhibit tumor growth?
Break of tolerance toward native forms of citrullinated autoantigens may lead to reactivity against citrullinated autoantigens via epitope spreading [ 33].
Upregulation of skin-specific autoantibodies may indicate that early events in the break of tolerance take place in cutaneous structures.
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