This direct or indirect interaction between pathogen effectors and their cognate host resistance (R) proteins/'guardee' proteins activates host defence mechanism, controlling host resistance (Stergiopoulos and de Wit 2009).
The development of cartilage injury-induced arthritis involves a series of immune responses that mobilize various types of immune cells into the wound site and activate host defences and tissue repair.
These cytokines and chemokines also function as central mediators in activating various host defence systems such as apoptosis, JAK/STAT signalling pathway, mitogen activated protein kinase (MAPK) signalling pathway and ultimately trigger the appropriate adaptive immune system.
Many of the immune activating abilities of LPS can be attributed to the lipid A unit, which binds to the toll-like receptor 4 (TLR4), and activates the host defence effector system by rapidly triggering pro-inflammatory processes [ 12- 15].
The innate immune system is the first line of host defence against pathogens and is activated by host recognition of conserved pathogen-associated molecular patterns (PAMPs).
Some bacteria have developed mechanisms to evade or exploit the processes activated by ubiquitination, producing both ubiquitin ligases and deubiquitinases that modulate host defence responses.
Stress activated mobilization of these elements by failure of epigenetic silencing (the host defence model of repressing the movement of mobile elements; [ 42, 43]) can lead to (re)activation of mobile elements and consequently to major and rapid genome alterations [ 40, 41, 44, 45].
Thus, the ability of pilin to activate the inflammasome as described here can play an additional role in host defence against a range of bacteria.
Mannose binding Lectin (MBL) mediates protection against infections by activating the complement system, but certain microorganisms may increase infectivity by exploiting this host defence system.
The alternative pathway mediates the role of complement protein in host defence against C. neoformans, although nonencapsulated cryptococci are able to activate the classical pathway (Kozel et al., 1991; Mershon-Shier et al., 2011).
