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After all, to persist in the brain for many years, T. gondii must not do too much damage to its host, continually stimulating the release of anti-inflammatory molecules which limit tissue damage while letting the infection persist.
The aim of inflammation is to limit tissue damage through phagocytosis.
We propose that the aim of this extensive network is to limit tissue damage while enabling an IFN response that is temporally appropriate and of sufficient magnitude.
In chronic infectious diseases, Tregs dampen inflammation to limit tissue damage, but they can also inhibit ensuing effector immunity, thereby impairing pathogen clearance.
As no curative solution is currently available, treatment of BD attempts to relieve symptoms, resolve inflammation, limit tissue damage, reduce recurrence frequency and severity, and avoid life-threatening complications.
This review describes targeted strategies to modulate the immune response in order to limit tissue damage following injury, promote an anti-inflammatory environment that leads to regeneration, and induce antigen (Ag -specific tolerAg -specificn tolerancegenerathat diseases that destroy tissues and promote engraftment of transplanted canls.
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Together, these studies support the notion that ROCK1 may represent an attractive therapeutic target to limit tissue damages due to increased apoptosis under certain pathological conditions.
In conjunction with their role in host defense, TLRs also play concomitant roles limiting tissue damage and promoting wound healing at sites of injury.
We also report that in the lung compartment the high responder IL10 −1082 AAhi may play a critical role in limiting tissue damage in PTB.
While our data suggest that IL-22 is not required for bacterial clearance during systemic or mucosal LM infection, other models have found that IL-22 protects cells from apoptosis, thereby limiting tissue damage [26], [27], [32], [33].
They are also responsible of limiting tissue damage during ongoing and resolving immune responses [ 17, 18].
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