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Decreased IL-12 levels may contribute to the pathogenesis of NEC by allowing bacteria to escape host defenses.
Advances in tumor biology and tumor immunity have helped to better understand the mechanisms displayed by a number of tumors to escape host immunity.
Recent studies in preclinical models and HCV-infected patients have demonstrated that the virus has developed multiple strategies to escape host immune responses during viral entry.
It has become a truism that these polymorphisms are the outcome of selective pressure on S. pneumoniae to escape host immunity.
Our findings provide the most detailed structural understanding of periplasmic flagella and the surrounding cell envelope, which enable this enigmatic bacterium to efficiently penetrate tissue and to escape host immune responses.
However, even among highly expressed genes there are mRNAs that escape host shutoff.
In addition, GAS down regulates multiple cell surface proteins, presumably to escape host immune recognition.
Among the 31 rickettsial genes up-regulated in eschars, several are plausibly involved to escape host response.
In this study we focused on the mechanisms that B. pertussis employs to escape host immune responses and the role played by CyaA.
Previous studies have identified cellular genes that are either targets of or escape host shutoff during viral infection [5], [10], [11].
The capsular antigen F1 on plasmid pMT1 and the pH 6 antigen promote resistance to phagocytosis and help the bacteria escape host defense mechanisms [37], [38].
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