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B. pertussis infection or pertussis vaccination of mice also induced an IL-17 response that was dependent on TLR4 signaling and IL-1, and that contributed to protection against B. pertussis challenge [16], [20].
Moreover, injection of modified cells from these animals into healthy mice also induced symptoms in the recipients.
Plasma-derived MVs from MRL/lpr mice also induced the production of IL-6 and TNF-α, while MVs from BALB/c mice induced only a small increase.
The transfer of CD4+CD25+ T cells from EPIT-treated mice also induced a low but significant increase in the proportion of spleen Tregs in recipient mice P < 0.01 (Fig. 7b).
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Passive transfer of serum containing arthritogenic autoantibody from K/BxN mice into normal mice also induces arthritis [ 23, 24].
In addition, S377-588-Fc elicited higher-titer neutralizing antibodies than all the other RBD fragments in mice, and also induced high-titer neutralizing antibodies in immunized rabbits.
The kdhAB mutant of F. tularensis LVS strain not only was significantly attenuated in mice, but also induced an early innate immune response both in vitro and in vivo.
In addition, all TEPITOPE-selected HIV-1 peptides were predicted to bind to H-2d class II molecules, and immunization of BALB/c (H-2d) mice with HIVBr18 also induced broad specific T cell responses to predicted peptides (unpublished observations).
In these control mice autophagy was also induced as shown by an increase in LC3-II, Beclin-1, and BNIP3 when compared to the GAA+/− (Figures 4A and 4B).
We found that in C57BL/6 mice, TNF autovaccination also induced high levels of anti-TNF antibodies in the serum that plateaued 8 weeks after immunisation.
Not only this, but Halder et al. (1995a) showed that the Pax6 gene from mice could also induce the generation of eyes in flies but not mouse eyes, fly eyes (Fig. 15).
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