Lottery Action, January 26 - February 6, 2005, Vol. 12, No. 2

Iowa Lottery Newsletter for Retailers

Catalogue de tableaux provenant de la gallerie et du cabinet de M. le Baron de Banckheim, qui seront vendus le mercredy 12 avril 1747...

[Vente (Art). 1747-04-12. Paris]

Lottery Action, February 7-20, 2005, Vol. 12, no. 3

Iowa Lottery newsletter for Lottery retailers.

Lottery Action, February 21-March 6, 2005, Vol. 12, no. 4

Iowa Lottery Newsletter for Lottery Retailers

Lottery Action, March 3-7, 2005, Vol. 12, no. 5

Lottery Newsletter for Retailers

Lottery Action, March 21-April 3, 2005, Vol. 12, no.6

Lottery Newsletter for Retailers

Lottery Action, April 4-17, 2005, Vol. 12, no. 7

Lottery Newsletter for retailers

Natural killer-like T cells develop in SJL mice despite genetically distinct defects in NK1.1 expression and in inducible interleukin-4 production.

An unusual subset of mature T cells expresses natural killer (NK) cell-related surface markers such as interleukin-2 receptor beta (IL-2R beta; CD122) and the polymorphic antigen NK1.1. These "NK-like" T cells are distinguished by their highly skewed V alpha and V beta repertoire and by their ability to rapidly produce large amounts of IL-4 upon T cell receptor (TCR) engagement. The inbred mouse strain SJL (which expresses NK1.1 on its NK cells) has recently been reported to lack NK1.1+ T cells and consequently to be deficient in IL-4 production upon TCR stimulation. We show here, however, that SJL mice have normal numbers of IL-2R beta+ T cells with a skewed V beta repertoire characteristic of "NK-like" T cells. Furthermore lack of NK1.1 expression on IL-2R beta+ T cells in SJL mice was found by backcross analysis to be controlled by a single recessive gene closely linked to the NKR-P1 complex on chromosome 6 (which encodes the NK1.1 antigen). Analysis of a panel of inbred mouse strains further demonstrated that lack of NK1.1 expression on IL-2R beta+ T cells segregated with NKR-P1 genotype (as assessed by restriction fragment length polymorphism) and thus was not restricted to the SJL strain. In contrast, defective TCR induced IL-4 production (which appeared to be a unique property of SJL mice) seems to be controlled by two recessive genes unlinked to NKR-P1. Collectively, our data indicate that "NK-like" T cells develop normally in SJL mice despite genetically distinct defects in NK1.1 expression and inducible IL-4 production.

Lottery Action, May 2-12, 2005, Vol. 12, no. 9

Iowa Lottery Authority Retailer Newsletter

Lottery Action, May 16-June 5, 2005, Vol. 12, no. 10

Iowa Lottery Authority Retailer Newsletter

Lottery Action, June 6-19 2005, Vol. 12, no. 11

Iowa Lottery Retailer Newsletter

Lottery Action, March 21-April 3, 2005, Vol 12, No. 6

Iowa Lottery Retailer Newsletter

MyD88, an adapter protein involved in interleukin-1 signaling.

MyD88 has a modular organization, an N-terminal death domain (DD) related to the cytoplasmic signaling domains found in many members of the tumor necrosis factor receptor (TNF-R) superfamily, and a C-terminal Toll domain similar to that found in the expanding family of Toll/interleukin-1-like receptors (IL-1R). This dual domain structure, together with the following observations, supports a role for MyD88 as an adapter in IL-1 signal transduction; MyD88 forms homodimers in vivo through DD-DD and Toll-Toll interactions. Overexpression of MyD88 induces activation of the c-Jun N-terminal kinase (JNK) and the transcription factor NF-kappaB through its DD. A point mutation in MyD88, MyD88-lpr (F56N), which prevents dimerization of the DD, also blocks induction of these activities. MyD88-induced NF-kappaB activation is inhibited by the dominant negative versions of TRAF6 and IRAK, which also inhibit IL-1-induced NF-kappaB activation. Overexpression of MyD88-lpr or MyD88-Toll (expressing only the Toll domain) acted to inhibit IL-1-induced NF-kappaB and JNK activation in a 293 cell line overexpressing the IL-1RI. MyD88 coimmunoprecipitates with the IL-1R signaling complex in an IL-1-dependent manner.