Immune Defences of Teleost Fish - Aquaculture Nutrition: Gut Health, Probiotics and Prebiotics - page 38

bacterial PAMPs via TLRs 1, 2, 4, 9 and NOD1 and NOD2, whereas TLRs 3, 7, 8 and 9
recognize viral PAMPs. These innate responses to intracellular pathogens facilitate activation
and programming of the slower adaptive cell-mediated immune responses. CMI is involved in
defence against intracellular pathogens by mounting cytotoxic responses. APCs present anti-
gen in the context of both MHC I and MHC II: antigenic peptide presented by MHC I restricts
T C -mediated responses which kill infected host cells via perforin and granulolysin, whereas
MHC II antigen activates Th 1 cells that induce either a DTH response through cytotoxic
activity of activated macrophages or T C activation through Th 1 -speciic effector cytokines.
In addition, these pathogens may initiate Th 17 activity via IL-23 etc., resulting in activation of
neutrophil/granulocytic cytotoxic cells. Extracellular-resident pathogens such as the intestinal
helminth Pomphorhynchus laevis and fungi do not hide inside host cells and are thus gen-
erally visible to immune defences. The innate immune system recognizes these PAMPs via
an array of receptors which include MBL, dectin-1, TLRs 2, 4, 5 and NLRs; these are capa-
ble of mounting cytotoxic, inflammatory, phagocytic and humoral responses. Such humoral
factors involved in these responses to extracellular pathogens include immunoglobulin pro-
duction. MHC II-restricted antigen recognition in the context of IL-4/IL-5/IL-13 primes for
aTh 2 -mediated B cell activation and antibody production. These antibodies are likely to be
involved in a range of functions which include neutralization, tagging for phagocytotic clear-
ance, complement activation and antibody-dependent cell cytotoxicity (ADCC).
Dependent on the immune response elicited to a defined pathogenic infection, the host
fish may clear the pathogen and return to a state of well-being, or can deteriorate, either as a
consequence of over-growth of the pathogen or as a result of inappropriate or over-exuberant
immune responses leading to host-driven immunopathology. This over-exuberant response is
likely to result in a tissue-destructive hypersensitivity or inflammatory response, ultimately
manifesting as deep ulcerations and tissue/organ failure with consequences for the ability of
the fish to thrive. Such an allergic/hypersensitivity response, for example, may result from the
release of helminth worms from cysts; the immediate massive antigenic challenge resulting
from release of massive numbers of worms present in a cyst induces a massive Th 2 -driven
allergic response which is more harmful to the host. The ensuing degranulation responses
create a proteolytic and inflammatory environment which has devastating consequences for the
fish host tissue. The efficient mounting of an immune response to a pathogen which presents
early and in controllable numbers is desirable but unrealistic. The pathogen itself would rather
hide or employ mechanisms of immune evasion, until such time that it is powerful enough,
or present in sufficient numbers, that it can expose itself to host immune reactions during the
process of translocation and reinfection of fresh host tissue.
The immune fight which ensues between host teleost fish and pathogen is a real dynamic
battle. It is not merely a matter of the host mounting an anti-pathogen immune response,
capable of recognition, killing and clearance. To understand any battle between host protection
and pathogen infection, it is necessary to think of this situation as a bidirectional fight between
host and pathogen. Let battle commence! In addition to the immune response, integral to
the outcome of the fight is the ability of the pathogen to counteract the host's immune
response; this is achieved by specialist and often pathogen-specific mechanisms that can
either deviate, suppress or evade the host's responses. These evasion techniques (or pathogen
escape mechanisms) are varied; any successful fish pathogen may have one or a collection of
immune-evasion responses. These evasion responses are likely to include hiding from host