In animal models it is often possible to block Th1-mediated autoimmunity by deviating the response to Th2. In this article, Graham Rook and colleagues argue that this might prove a dangerous strategy in humans, and that we should distinguish between potentially pathogenic Th2 effector cells, and Th2-like physiological regulators of Th1 responses. The regulators might be triggered by appropriate Th1-inducing bacterial vaccines.
The two polarized T helper (Th) subsets Th1 and Th2 are identified by their signature cytokines, interferon γ (IFN-γ) and interleukin 4 (IL-4) respectively. Understanding the transcriptional regulation of cytokine expression is therefore critical for elucidating the process of Th cell differentiation. Ubiquitous and tissue-specific transcription factors, as well as chromatin remodeling of genomic loci have been implicated in IL-4 and IFN-γ regulation. We propose a model of Th1/Th2 polarization based on the balance between Th1- and Th2-specific transcription factors.
The vertebrate immune system recognizes bacterial DNA as foreign based on its content of unmethylated CpG motifs. The detection of CpG motifs by the innate immune system induces immune responses that are strongly Th1-biased. These responses can be mimicked using synthetic oligonucleotides, which have shown significant effects as vaccine adjuvants and as immunotherapeutics for treatment of cancer and allergic conditions in model systems.
Immunosenescence is a complex process involving multiple reorganizational and developmentally regulated changes, rather than simple unidirectional decline in all functions. Here, these compensatory modulations are reviewed with reference to the importance of integrating information on cellular alterations identified in vitro with data on global physiological changes in the aged environment with which these cells interact in vivo.
A recent conference* on tumour necrosis factor (TNF) and related molecules highlighted the many recent advances, from intracellular signalling to clinical applications, in our knowledge of this fascinating molecule.
‘It is not the strongest of the species that survives, nor the most intelligent; it is the one that is most adaptable to change.’
Charles Robert Darwin (1809–1882)
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