01736nas a2200217   4500000000100000008004100001260001200042653002700054653002200081653001700103100001600120700002000136700002200156700002100178245011300199856004700312300001200359490000700371520112600378022001401504       2021                            d  bMDPI AG10aMicrobiology (medical)10aMolecular Biology10aMicrobiology1 aGuerrero GG1 aRangel-Moreno J1 aIslas-Trujillo SO1 aRojas-Espinosa O00aIntramuscular Boosting with hIFN-Alpha 2b Enhances BCGphipps-Induced Protection in a Murine Model of Leprosy  uhttps://www.mdpi.com/2036-7481/12/3/51/pdf  a711-7260 v123 a<jats:p>Host immunity to Mycobacterium leprae encompasses a spectrum of mechanisms that range from cellular immunity-driven protection to damage associated with humoral immunity as in type-2 leprosy reactions. Although type I interferons (IFNs) participate in eliminating intracellular pathogens, their contribution to the production of antibodies and CD3+ FOXP3+ regulatory T cells (Tregs) in BCG vaccine-mediated protection in leprosy is unknown. BCGphipps (BCGph) priming followed by intramuscular hIFN-α 2b boost significantly reduced lesion size and Mycobacterium lepraemurium growth in the skin. T follicular regulatory cells (TFR), a subset of Tregs induced by immunization or infection, reside in the germinal centers (GCs) and modulate antibody production. We found impaired Treg induction and improved GCs in draining lymph nodes of BCGph primed and hIFN-α 2b boosted mice. Moreover, these mice elicited significant amounts of IL-4 and IL-10 in serum. Thus, our results support the adjuvant properties of hIFN-α 2b in the context of BCGph priming to enhance protective immunity against skin leprosy.</jats:p>  a2036-7481