By Frederick W. Alt
Advances in Immunology, a normal and hugely revered booklet, provides present advancements in addition to accomplished reports in immunology. Articles tackle the wide variety of subject matters that include immunology, together with molecular and mobile activation mechanisms, phylogeny and molecular evolution, and scientific modalities. Edited and authored by means of the major scientists within the box, every one quantity offers updated details and instructions for destiny examine.
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Extra resources for Advances in Immunology, Vol. 97
Chemokine-stimulated T cells rapidly polarize, forming a leading F-actin-rich edge directed toward the source of stimulus, and a trailing uropod projection. This leading edge and uropod, along with a central polarizing region, serve as subcellular compartments for the polar distribution of various organelles, lipid rafts components, receptors, and signaling molecules during migration (Box A, leading edge components; Box B, central polarizing compartment; Box C, uropodal components). Chemokine receptors and integrins, which localize to the leading edge of migrating T cells, sense chemoattractant gradients and allow adherence to the substratum, respectively.
2003). , 1998). , 1998). , 2002, 2007). , 2002). Thus, based on this molecular polarity, the F-actin-dependent formation of an extended leading edge is critical for recognizing gradients through specialized chemosensory receptors, promoting integrin-mediated adhesion and providing contractile potential at F-actin anchored adhesion sites, which allow migrating cells to pull themselves forward (Fig. 5). Migrating T cells also form a posterior protrusion called a uropod. Although the exact role of this appendage remains elusive, and is less well defined than the leading edge, the finding that various molecules selectively compartmentalize into the uropod has begun to shed light on mechanisms underlying its formation and function.
2007). Activation of RAP1, which is required for T cell polarization, leads to localized activation of CDC42, the major activator of the PAR polarity complex. Moreover, RAP1-induced T cell polarization is impaired by expression of DN-CDC42 or RNAi-depletion of PAR-3, suggesting that the PAR complex is essential for RAP1-regulated polarity. In addition, RAC1mediated cytoskeletal remodeling is necessary for RAP1-induced polarization, and RAC1 activation requires both CDC42 and the PAR polarity complex.
Advances in Immunology, Vol. 97 by Frederick W. Alt