Page 852 - Veterinary Immunology, 10th Edition
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VetBooks.ir  Evasion of the Immune Response





               The outcome of any infection depends upon the continuously
               evolving battle between the host and the microbe. To survive

               within an animal, bacteria must evade or inhibit the immune
               defenses. The complex interrelationships between bacteria and their
               animal hosts, described in Chapter 21, include the role of
               commensal bacteria on mucosal surfaces in regulating the growth
               and development of the immune system. These bacteria generally

               do not aggressively seek to invade the body, so equilibrium can be
               achieved. Nevertheless, an invading microorganism becomes a
               pathogen because it can invade the body, evade the immune

               defenses, and survive at least for a time within its host. Pathogenic
               bacteria, like all organisms, try to avoid destruction. They have
               evolved many different mechanisms to overcome host innate and
               adaptive immune responses.



               Evasion of Innate Immunity


               The key to successful microbial invasion, at least initially, is
               evading innate immunity. Bacteria employ diverse mechanisms to
               prevent or at least delay an unpleasant fate. Only some selected

               examples can be mentioned here.
                  For example, some bacteria interfere with TLR signaling
               pathways and inflammasome activation (Fig. 26.5). The methods
               used include the production of modified PAMPs that will not

               trigger TLRs, masking of PAMPs, blockage of TLR signaling
               pathways, destruction of signaling molecules, destruction of NF-κB,
               and misdirection of signaling pathways toward antiinflammatory
               pathways. Thus M. tuberculosis uses a masking lipid to cover its

               PRRs. Leptospira have lipopolysaccharides that are recognized by
               TLR2, but not by TLR4. Campylobacter jejuni makes a form of
               flagellin that is not recognized by TLR5. Yersinia pestis reduces
               acetylation of lipid A so that it cannot be recognized by TLR4.

               Bacteria also differ in the amount of CpG dinucleotides in their
               DNA, and so differ in their ability to trigger TLR9. Potent
               stimulators of TLR9 include M. tuberculosis and Pseudomonas





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