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Years and Volumes

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Molecular Medicine Volume 12

Articles from this Volume

2006 Supplement 
 
The function of the mammalian immune system is to detect and destroy foreign antigens from viruses, bacteria and other exogenous sources; as well as dysfunctional or aberrant endogenous antigens, such as cancer cells.  In this capacity, cells of the immune system can have highly lethal effects on its targets, a characteristic that allows rapid and efficient clearance of undesired cells, microorganisms, and antigens.  Left uncontrolled, however, these lethal activities can have adverse effects on normal cells and tissues, causing pathologies ranging from rheumatoid arthritis, inflammatory bowel disease and septic shock, to lupus, myeloma and leukemia.  In order to maintain the proper balance between healthful and harmful immune responses, the cells of the immune system rely on complex direct and indirect interactions that are mediated in part through cell surface molecules including some known as cellular differentiation (CD) markers. Over 500 leukocyte CD markers have been characterized to date.  These surface proteins serve as the interface between the immune cells and their environment, and occupy a central role in transducing intracellular signals that regulate cellular activities.  Among these cell surface proteins are two members of a family of cyclases that metabolize nicotinic adenine dinucleotide (NAD+) into nicotinic acid adenine dinucleotide phosphate (NAADP) and cyclic adenosine dinucleotide phosphate-ribose (cADPR), and are potent modulators of the immune system.  These two ectoenzymes, known as CD38 and CD157, have been the focus of much research into the biology of the immune system.  Research being conducted by molecular biologists, protein chemists, immunologists and clinicians has generated a better understanding of the biological functions of the CD38 family of ectoenzymes, and their roles in health and disease.  Discoveries in basic biology, combined with clinical observations and ground-breaking translational research, are setting the stage for targeted therapeutics, and fulfilling the mission of molecular medicine. As presented at the Torino CD38 Meeting, the culmination of these efforts is the identification of these ectoenzymes as potential new therapeutic targets or diagnostic markers for myleoma and leukemia.

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Posted by Leah Caracappa on Dec 6, 2006 12:00 AM CST
Fabio Malavasi, Silvia Deaglio, Enza Ferrero, Ada Funaro, Jaime Sancho, Clara M Ausiello, Erika Ortolan, Tiziana Vaisitti, Mercedes Zubiaur, Giorgio Fedele, Semra Aydin, Elena V Tibaldi, Ilaria Durelli, Riccardo Lusso, Franco Corzo, and Alberto L Horenstein

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Posted by Leah Caracappa on Dec 5, 2006 12:00 AM CST
Posted by Leah Caracappa on Dec 4, 2006 12:00 AM CST
Richard A Billington, Santina Bruzzone, Antonio De Flora, Armando A Genazzani, Friedrich Koch-Nolte, Mathias Ziegler, and Elena Zocchi

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Posted by Leah Caracappa on Dec 3, 2006 12:00 AM CST
Posted by Leah Caracappa on Dec 2, 2006 12:00 AM CST
Posted by Leah Caracappa on Dec 1, 2006 12:00 AM CST
Amy Warenda Czura and Christopher J Czura

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Posted by Leah Caracappa on Nov 7, 2006 12:00 AM CST

Fabio Ghiotto, Franco Fais, Emilia Albesiano, Cristina Sison, Angelo Valetto, Gianluca Gaidano, Janine Reinhardt, Jonathan E Kolitz, Kanti Rai, Steven L Allen, Manlio Ferrarini, and Nicholas Chiorazzi

Analyses of immunoglobulin (Ig) VHDJH rearrangements expressed by B-CLL cells have provided insights into the antigen receptor repertoire and maturation stages of B-lymphocytes that give rise to disease.  As Ig variable (V) domains are the components of the B-cell antigen receptor that interact with antigen, the analyses of gene segments that encode these domains can provide indirect information about the structure of the B-cell antigen receptor.  Ghiotto et al. (300-308) analyzed the VL and JL gene segments of 206 B-CLL patients, paying particular attention to the frequency of use and association, mutation status, and LCDR3 characteristics.  The similarities and differences observed between the IgH and IgL V gene repertoires expressed in B-CLL suggest some novel features while also reinforcing concepts derived from studies of the IGH repertoire.

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Posted by Leah Caracappa on Nov 5, 2006 12:00 AM CST

Charles H Lang and Robert A Frost

Alternatives in protein metabolism during sepsis include both decreased protein synthesis as well as increased protein degradation, resulting in weight loss during the course of the disease.  Leucine availability represents an important nutritional signal responsible for postprandial stimulation of muscle protein synthesis.  Sepsis blunts leucine’s nutrient signaling ability by impairing the initiation of translation, resulting in decreased skeletal muscle protein synthesis.  Here Lang and Frost (291-299) test whether overproduction of the catabolic mediators, tumor necrosis factor alpha (TNFα) or glucocorticoids, mediate sepsis-induced leucine resistance.  Results demonstrate that sepsis-induced leucine resistance in skeletal muscle results from the cooperative interaction of both TNFα and glucocorticoids. These findings extend the knowledge base surrounding sepsis-induced leucine resistance and may initiate therapeutic approaches targeting both catabolic mediators simultaneously.

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Posted by Leah Caracappa on Nov 4, 2006 12:00 AM CST

Davorka Messmer, Ikusuke Hatsukari, Naoko Hitosugi, Ingo G H Schmidt-Wolf, and Pravin C Singhal

While our understanding of the role of opiates in the modulation of immunity has expanded, the direct effect of morphine on immunity remains enigmatic.  Opiate addicts are prone to infection often attributed to immunomodulatory effects and chronic administration affects both innate and adaptive immunity. There is growing evidence that opioid receptors are expressed by cells of the immune system and may modulate immune responses.  Dendritic cells play a central role in the initiation and control of the adaptive immune response. Here, Messmer et al. (284-290) investigate the effects of morphine on the differentiation process of human myeloid dendritic cells from monocytes. Results indicate that the signals for pain and immunomodulation are intricately linked.  These data advance our understanding of the mechanism of opiates in the adaptive immune response.

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Posted by Leah Caracappa on Nov 3, 2006 12:00 AM CST
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