By Martin Turner (auth.), Bali Pulendran, Peter D. Katsikis, Stephen P. Schoenberger (eds.)
This quantity offers a suite of studies derived from paintings offered on the Aegean convention: “3rd Crossroads among innate and adaptive immunity” which happened in the course of September 27 - October 2, 2009 on the Minoa Palace convention heart in Chania, Crete, Greece. This assembly was once the 3rd in a chain, and assembled a group of scientists engaged on mechanisms through which the innate immune approach of the host senses pathogens, the mobile and signaling networks that orchestrate the innate reaction and antigen presentation and adaptive immunity. many of the features of the innate reaction, together with dendritic cells, T cells, B cells, NK cells, NK-T cells and the supplement cascade throughout the host reaction to pathogens and tumors is barely now growing elucidated. The respective fields that target those immune cells and molecules have tended to be particularly compartmentalized, and but rising proof issues to the interconnectedness of those elements in coordinating the innate reaction, and its next influence at the adaptive reaction. The objective of this convention was once to start up cross-talk among those different immunological fields, and advertise and facilitate dialogue at the interactions among the innate immune reaction and the adaptive immune reaction and finally facilitate collaboration among those components of research. Following at the footsteps of the exceptional good fortune of its precursors, the “3rd Crossroads among Innate and Adaptive Immunity” Aegean convention used to be hugely winning in bringing jointly and connecting scientists and specialists from worldwide to deal with serious components of Innate and Adaptive immunity.
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Extra resources for Crossroads Between Innate and Adaptive Immunity III
Therefore, the licensing hypothesis is not sufficient to explain NK cell functionality during viral infection. 1 Introduction Natural Killer (NK) cells play a crucial role in controlling certain viral infections and eliminating tumor cells. Depletion of NK cells renders animals susceptible to infections such as mouse cytomegalovirus (MCMV), ectromelia virus, and Ebola virus [1–3]. Humans preferentially lacking NK cell functions are unable to control Epstein-Barr virus, human cytomegalovirus, and varicella zoster virus, among others [4–6].
2 The “Missing Self ” Hypothesis and NK Cell Self-tolerance Control of NK cell activation is now understood to be a highly complex system of diverse inhibitory and activating receptor-ligand interactions. NK cells achieve inhibition mainly through interaction with MHC class I molecules via NK cell receptors that suppress rather than activate NK cell function. These receptors mediate a regulatory mechanism that is thought to protect normal cells from autologous NK cell attack. Lack of engagement of inhibitory receptors, along with the engagement of activating receptors by activating ligands on potential target cells results in target cell killing [12–14].
Mayoral RJ, Pipkin ME, Pachkov M, van Nimwegen E, Rao A, Monticelli S (2009) MicroRNA-221-222 regulate the cell cycle in mast cells. Muljo SA, Ansel KM, Kanellopoulou C, Livingston DM, Rao A, Rajewsky K (2005) Aberrant T cell differentiation in the absence of dicer. Natkunam Y, Farinha P, Hsi ED, Hans CP, Tibshirani R, Sehn LH, Connors JM, Gratzinger D, Rosado M, Zhao S, Pohlman B, Wongchaowart N, Bast M, Avigdor A, Schiby G, Nagler A, Byrne GE, Levy R, Gascoyne RD, Lossos IS (2008) LMO2 protein expression predicts survival in patients with diffuse large B-cell lymphoma treated with anthracycline-based chemotherapy with and without rituximab.
Crossroads Between Innate and Adaptive Immunity III by Martin Turner (auth.), Bali Pulendran, Peter D. Katsikis, Stephen P. Schoenberger (eds.)