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After a century of analysis, a number of strains of facts now point out that the facility of adenosine to without delay regulate inflammatory cells has a tremendous influence at the features of the inflammatory and immune structures. for that reason, many promising healing methods are commencing to emerge that concentrate on the modulation of adenosine, together with the advance of compounds that intrude with the breakdown of adenosine, in addition to particular agonists and antagonists of assorted adenosine subtypes.
The Cardiac MRI in prognosis, scientific administration and analysis of Arrhythmogenic correct Ventricular Cardiomyopathy / Dysplasiaprovides up to date information about the simplest diagnostic protocols and CMR sequences for the assessment of sufferers with suspected or identified ARVC/D. It contains CMR protocol summaries and medical algorithms provided as circulate diagrams, a lot of that have by no means been formerly released.
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Extra resources for Annual Review of Immunology Volume 23 2005
Conversely, transgenic expression of OX40L in C57BL/6 mice, which normally control Leishmania, resulted in an elevated Th2 response and decreased parasite clearance (138). Role of OX40/OX40L in Autoimmune and Inflammatory Reactions A large body of evidence suggests that OX40-OX40L interactions play a role in autoimmunity and inflammation. OX40-OX40L interaction is required for the induction of EAE in mice, and depletion of OX40+ T cells or preventing OX40OX40L interactions ameliorates disease (121, 129, 154, 155).
The absence of OX40 does not in itself appear to induce tolerance (159). However, provision of agonistic anti-OX40 can reverse T cell anergy induced in vivo by peptide administration (161). Interestingly, transfer of self-specific CD4 T cells into recipient mice induces expansion of T cells, which remain anergic. However, concomitant administration of agonistic anti-OX40 antibodies relieves these self-specific T cells from their anergic state, resulting in autoimmunity and death of the anti-OX40-treated recipient mice (162).
On T cells, constitutive overexpression of OX40L results in accumulation of CD4 effector T cells, increased CD4 T cell responses, as well as an autoimmune phenotype characterized by inflammation of the lung and intestine, with no change in CD8 populations (148). Thus, both gene-targeted and transgenic mice support a role for OX40 primarily on CD4 T cells. There are conflicting data on the effect of OX40 or OX40L deficiency on B cell responses in mice. Three studies showed no defect in antibody responses to both protein and infectious agents (KLH, VSV, influenza virus, L.
Annual Review of Immunology Volume 23 2005 by Annual Reviews