Article Text

Inflammatory processes: molecular mechanisms and therapeutic opportunities
  1. University of Helsinki
  2. Central Hospital and Invalid Foundation
  3. Helsinki, Finland
  4. yrjo.konttinen{at}

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Inflammatory processes: molecular mechanisms and therapeutic opportunities. Eds L Gordon Letts Jr, Douglas W Morgan. (Pp160; DM198.) Basel: Birkhauser Verlag AG, 2000. ISBN 3-7643-6025-9.

Presentations and workshops held from 1 to 5 November 1998, at the 9th International Conference of the Inflammation Research Association at Hershey Lodge and the Convention Centre at Hershey, Pennsylvania, are the basis of this book. It deals particularly with molecular mechanisms of inflammation and therapeutic opportunities. It is mainly suitable for colleagues in rheumatology who are engaged in inflammation research and also for those who want to look ahead at new targets for treatment. It is too detailed for the regular rheumatologist and out dated for those at the frontier of research.

Information is provided on some aspects of inflammation, which are usually not dealt with in rheumatological meetings. Particularly, the chapters dealing with signal transduction downstream from TNF/TNF-R and IL1/IL1R interactions are quite interesting. The JNK MAP kinases which play a part in the regulation of AP-1 transcription activity are discussed in some detail. Structural organisation of the JNK signalling pathway and involvement of scaffold proteins are described. Similarly, in NF-6B-inducing kinase (NIK), I6B kinases (IKK-α and IKK-β), ubiquitination of phosphorylated I6B and proteasome mediated degradation of ubiquitinated I6B are described as potential targets downstream TNF/TNFR and IL1/IL1R interactions. Small molecular regulators of AP-1 pathway, such as inhibitors of the ERK cascade, JNK inhibitors, and inhibitors of p38 activity are described. Antioxidants and free radical scavengers can block NF-6B activation. Interestingly for rheumatologists, salicylates have been recently shown to be specific inhibitors of IKK2.

In addition to TNF/TNF-R and IL1/IL1R interactions the effects of cyclosporin A and cyclophylin-A complex and FK506 and FKBP12 complex on calcineurin are dealt with, as is the effect of rapamycin and FKBP12 complex on mammalian target of rapamycin (mTOR).

In addition, there are chapters on chemokines, particularly those acting on eosinophils and those which have a role in asthma and allergy. The role of lymphotoxin, in particular the role of the heterotrimeric LTα1β2 on LTβR, on lymphoid tissue formation is discussed.

At the end of the book, there are short references to special workshops dealing with targets in rheumatoid arthritis and osteoarthritis, mediators of inflammation and their enzymes, cell adhesion molecules, and leucocyte trafficking and angiogenesis, wound repair, and skin inflammation.

People engaged in inflammation research will be interested in this book, though it derives from a meeting held in November 1998 and is not quite new any more. In addition, this is interesting reading for those rheumatologists who are interested in signal transduction initiated by and mediating the effects of tumour necrosis factor α, lymphotoxin, and interleukin 1, and the potent intracellular signalling molecules involved in it. However, because it consists of presentations and workshop reports, information is not provided in a structured way, but is somewhat fragmented, “caviar” for those who are already familiar with this field. Therefore, this book can be recommended to highly selected colleagues in the field of rheumatology.