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Brooks, stomatopods, and decapods: Crustaceans in research and teaching, 1878–1886
Published in Frank Truesdale, History of Carcinology, 2020
Although Claus decided that they are young Lysiosquillae they show their relationship to the genus Squilla as distinguished from Lysiosquillae by the following characteristics, all of which are shared by all fully-grown Alima larvae. The dactylus of the raptorial claw has on its inner edge a small number of marginal spines, usually about five or six; the hind body is wide and flat, and the postero-lateral angles of the abdominal somites end in acute spines. The outer edge of the proximal joint of the uropod is bordered by a small number of spines usually less than eight, and the inner one of the two spines on the ventral process from the posterior edge of the basal joint of the uropod is longer than the outer, and it has a tooth or lobe on its outer edge; and the telson has six marginal spines with minute secondary spines between the submedians, and four or more large secondary spines between the submedian and the second or intermediate, and usually a single one internal to the base of the third or lateral marginal spine. While it is true that all of these characteristics are not exhibited by every adult Squilla, there are no Stomatopods except those of this genus in which they are all united, and they are all of them present in most Squilla and in all the Alimae. (Brooks 1886).
Therapy with lnterleukin-2 and Tumor-Derived Activated Lymphocytes
Published in Ronald H. Goldfarb, Theresa L. Whiteside, Tumor Immunology and Cancer Therapy, 2020
When peripheral blood mononuclear cells (PBMC) are cultured in vitro for short periods of time (1–3 days) with interleukin-2 (rIL-2), dramatic morphological, biochemical, functional, and phenotypic changes occur. Close examination of an activated lymphocyte reveals a broad end, ruffled and organelle free, and a tapered end with a uropod containing a large population of granules (17). Biochemical changes in differentiating LAK cells include both an increase in the number of granules as well as an increase in granule associated serine esterases (18,19). PBMCs contain a subset of effector cells termed natural killer (NK) cells with the capacity to lyse the tumor cell line, K562 (20,21). Little or no lytic activity is detectable using unstimulated NK cells against the Daudi cell line or most other fresh or cultured tumor cell targets. In the presence of rIL-2, cytolytic activity is generated against Daudi and other tumor lines but not normal cells. Recent experiments in our laboratory have shown that a brief pulse in rIL-2 (15 min-1 hr) is all that is necessary for the delivery of the appropriate signal causing LAK precursors to develop cytotoxic potential (22). Maximum cytolytic potential was only achieved using PBMCs from cancer patients primed in vivo with rIL-2. Thus, LAK precursors are pre-activated in vivo with rIL-2 or other lymphokines generated during the priming process. This method of LAK-cell generation is now utilized in clinical trials (23).
Ultrastructural Studies on Mechanisms of Human Eosinophil Activation and Secretion
Published in Gerald J. Gleich, A. Barry Kay, Eosinophils in Allergy and Inflammation, 2019
Mature peripheral blood eosinophils (Fig. 1) are granulocytes with polylobed nuclei within which chromatin is generally condensed. Nucleoli are rarely present. Irregular, broad surface projections and, rarely, uropods characterize their surface profiles. The synthetic structures (Golgi, endoplasmic reticulum) are markedly reduced over their immature precursors. Cytoplasmic secretory granules of at least three types, in addition to nonmembrane-bound lipid bodies and vesiculotubular structures, characterize the remaining cytoplasmic organelles (1).
Using imaging to study inflammatory platelet–leukocyte interactions in vivo
Published in Platelets, 2020
Olivia Susanto, Michael J. Hickey
Due to the ease of imaging of this transparent vascular bed, intravital imaging of the cremaster muscle microvasculature has been commonly used for investigations of the fundamental mechanisms of leukocyte recruitment. This approach has generated key observations regarding platelet–leukocyte interactions during inflammation. Studies using rapid frame-rate imaging of platelets in the cremaster muscle revealed that platelet interactions with neutrophils did not necessarily require the neutrophil to be adherent, as neutrophils bearing adherent platelets were observed rolling along the endothelium [21]. In TNF-activated microvessels, platelet–neutrophil interactions were found to occur at both the leading edge and the CD62L-rich uropod, although interactions at the leading edge were more long-lived [19,41]. In contrast, in a model of bacterial lipopolysaccharide (LPS)-induced systemic inflammation, the uropod became the primary site for platelet–leukocyte interactions, due to PSGL-1 clustering at this location. Subsequently, PSGL-1 mediated interactions with activated platelets promoted neutrophil crawling and NET generation [19]. Via this platelet-dependent mechanism, neutrophils were able to scan the local microenvironment for inflammatory cues and then respond appropriately [19]. Platelet recruitment to the microvasculature is also induced in response to the chemokine CCL2, although in this case, this occurs independent of neutrophils and monocytes [40]. Under these circumstances, platelets adhere to the endothelium near endothelial cell junctions via a VWf-dependent mechanism. Subsequently, adherent platelets promote accumulation of both neutrophils and monocytes, thereby increasing the efficiency of leukocyte recruitment in this form of inflammation.
The pro-inflammatory role of platelets in cancer
Published in Platelets, 2018
Thrombi formation is one potential cause of inflammation in distant organs of cancer patients. A thrombus in the microvasculature will cause vessel occlusion and prevent normal blood flow. Reduced vascular perfusion will be sensed by the vessel wall and result in activation of the endothelium—a process that promotes inflammation. Upon endothelial activation, adhesion molecules responsible for capture and extravasation of leukocytes will be expressed. In a stepwise process, these endothelial receptors will allow leukocytes, such as neutrophils, to adhere to the endothelium, migrate through the vessel wall, and enter the tissue (16). The first response takes place only within minutes after endothelial activation is induced, when preformed P-selectin stored in Weibel Palade-bodies is released from endothelial cells and displayed on the endothelial surface (17). Leukocytes bind transiently and weak to selectins on the endothelium via P-selectin glycoprotein ligand-1 (PSGL-1) on their surface. In parallel, de novo formation of both P- and E-selectin is induced, together with integrin receptors such as intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). These CAMs are responsible for firm adhesion of the leukocytes, by interacting with integrins such as lymphocyte function associated antigen-1 (LFA-1) and macrophage-1 antigen (Mac-1). The integrin-mediated interactions will also induce signaling events in the endothelial cells leading to loosening of the endothelial junctions, facilitating transendothelial migration, and transcription of additional pro-inflammatory factors. The infiltrating immune cells will produce and secrete pro-inflammatory factors that will recruit more leukocytes to the site and hence exacerbate the inflammation. However, it may be worth to notice that platelets themselves actively participate in capturing of leukocytes. Activated platelets do also express receptors on their surface that allows direct interactions with immune cells, such as P-selectin and CD40L (18,19). A study by Sreeramkumar et al. exemplifies the significance of platelet P-selectin and leukocyte PSGL-1 in inflammation (20). It was shown that neutrophils that interact with activated endothelium polarize and protrude the trailing end of the cell body, the uropod, into the vessel lumen. The uropod contains PSGL-1 clusters that can “catch” activated platelets in the circulation expressing P-selectin. When this interaction takes place, the neutrophil is able to organize additional receptors needed for transmigration of the endothelium and initiate inflammation (20).