Th2–mediated host protective immunity to intestinal nematode infections

Intestinal nematode infections

Food limitation constrains host immune responses to nematode infections.

Trade-offs in the allocation of finite-energy resources among immunological defences and other physiological processes are believed to influence infection risk and disease severity in food-limited wildlife populations. However, this prediction has received little experimental investigation. Here we test the hypothesis that food limitation impairs the ability of wild field voles (Microtus agrest...

Host innate recognition of an intestinal bacterial pathogen induces TRIF-dependent protective immunity

Toll-like receptor 4 (TLR4), which signals through the adapter molecules myeloid differentiation factor 88 (MyD88) and toll/interleukin 1 receptor domain-containing adapter inducing IFN-β (TRIF), is required for protection against Gram-negative bacteria. TRIF is known to be important in TLR3-mediated antiviral signaling, but the role of TRIF signaling against Gram-negative enteropathogens is cu...

Macrophage apoptosis in host immunity to mycobacterial infections.

Macrophage apoptosis occurs within the granuloma, which is essential for successful immunity to tuberculosis. In vitro macrophage apoptosis is associated with the killing of intracellular Mycobacterium tuberculosis. A greater understanding of these observations will lead to new immunotherapies and improved vaccine design. The relevant apoptotic stimuli, the anti-mycobacterial mechanisms that th...

Intestinal nematode infections in children: the pathophysiological price paid.

The mechanism by which small animals such as rodents resist or eliminate nematode parasites requires mucosal inflammation as the final effector of the immune response. The resulting freedom from chronic infection may be worth the price of short-term illness. Putative vaccines which attempt to enhance the natural effect will have to take into account the inflammatory cost to the host. Human helm...