We hope for continuous EFIS-EJI support for future meetings, which is indispensable as it provides travel grants for a significant number of young immunologists who attend the conference. The next conference is planned for September 2012 and the details will be posted on http://www.img.cas.cz/tatra/ approximately one year in advance of the meeting. Perhaps we will see you there. Radek Špíšek Department of Immunology, Charles University, 2nd Faculty of Medicine, University Hospital Motol, Prague, Czech Republic e-mail: [email protected]

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“The behavior of self-reactive T cells 3-deazaneplanocin A mw in the peripheral immune system has often been studied by following the fate of adoptively transferred antigen-specific T cells in antigen expressing mice. In most cases, after a period of expansion, such cells undergo a slow clonal deletion, accompanied by the onset of anergy and/or suppression in the remaining cells. Here, we demonstrate that at initial frequencies approaching those found in normal repertoires, it is possible to completely avoid deletion Apoptosis inhibitor and still maintain peripheral tolerance. At starting numbers of <1000 T cells, stimulation by chronic self-antigens resulted in a period of robust clonal expansion, followed by a steady plateau phase extending

beyond 4 months. Despite their Bay 11-7085 stable persistence, the self-reactive T cells did not convert to a Foxp3+ fate. However, they displayed a considerable block in their ability to make IL-2, consistent with the onset of anergy — in a precursor frequency or deletion independent fashion. In an adaptive immune repertoire, the frequency of T cells that are specific for any given pathogen is thought to be very low. Although the precise numbers are difficult to estimate, in the mouse, it is thought to range in frequency from 1/1000 to 1/100,000 [1, 2] and numerically as low as 20 per mouse [3, 4]. The robust clonal expansion and differentiation that follows antigen recognition in vivo, is therefore geared to expanding

these rare precursors to large numbers of potent effector cells, in a short amount of time. However, the same process can be lethal if the target epitope is derived from a self-antigen. Therefore, the vertebrate has evolved several processes to curtail self-reactive T cells. After central tolerance deletes a large proportion of these, very few escape to the periphery. This makes it even more difficult to isolate and follow their behavior in unmanipulated animals (until an autoimmune process activates and expands them). Instead, we and others have routinely used adoptive transfer model systems that infuse a traceable population of self-reactive T cells into mice and follow their fate.