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Unlike traditional antibiotics, antimicrobial peptides can regulate the host immune system and kill bacteria directly (Gottler and Ramamoorthy 2009).
The HBeAg may function as a toleragen in utero and has been shown to regulate the host's immune response.
On the other hand, lipids can regulate the host response against Mtb.
Preceding or intercurrent viral infections may down regulate the host immune response leading to subsequent bacterial infection [25], [26].
As pointed out previously [17], [18], the parasitoid larvae need also to regulate the host development and consumes gently his body to avoid killing it too rapidly.
However, these results are in keeping with those of others that demonstrated the ability of T. gondii to potently regulate the host's immune response.
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In summary, we believe that there is some evidence suggesting that T. gondii may produce hairpins similar to its hosts and use them to regulate the hosts transcriptionally.
However, at the same time, a secreted fungal lipocalin was up-regulated (discussed above) implying that the parasite might be regulating the host's neuronal stress response.
The secretion of adrenal glucocorticoids subsequently down regulates the host inflammatory response, minimizing potential tissue damage.
Human NAIP regulates the host response to L. pneumophila infection and inhibits apoptosis or promotes pyroptosis in response to specific cellular signals (Katagiri et al., 2012).
The aim of this study was to determine the role of different toll-like receptors (TLRs) involved in regulating the host response to the S. suis infection and to speculate on differing mechanisms used by ST7 strains to induce disease.
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