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Immune System Imaging
Published in Margarida M. Barroso, Xavier Intes, In Vivo, 2020
Michael J. Hickey, M. Ursula Norman
Leukocyte migration is typically driven by interaction of chemokines with leukocyte-expressed chemokine receptors. In the cortex, chemokine expression is relatively low and uniform with CCL25 and CXCL12 contributing to DN thymocyte accumulation at the SCZ (Plotkin et al., 2003; Bunting et al., 2011; Dzhagalov and Phee, 2012). In the medulla, both the CCR4 ligands (CCL17, CCL22) and the CCR7 ligands (CCL19, CCL21) are highly expressed by medullary DCs, setting up a chemotactic gradient to attract cells expressing the appropriate receptors. After positive selection, thymocytes upregulate CCR4 and CCR7 allowing these cells to migrate into the medulla in response to this chemotactic gradient (Misslitz et al., 2006; Petrie and Zuniga-Pflucker, 2007). 2PM studies show that this migration is blocked by an inhibitor of chemokine receptor signaling. Similarly, positively selected thymocytes deficient in CCR7 showed reduced entry into the medulla following positive selection (Kurobe et al., 2006; Ehrlich et al., 2009), while CCR4 deficiency also reduced the ability of postpositive selection DP and SP CD4 thymocytes to accumulate in the medulla and to interact with medullary DCs (Hu et al., 2015). Together these observations support a role for chemokine-driven migration in these responses.
Tumor growth suppression by implantation of an anti-CD25 antibody-immobilized material near the tumor via regulatory T cell capture
Published in Science and Technology of Advanced Materials, 2021
Tsuyoshi Kimura, Rino Tokunaga, Yoshihide Hashimoto, Naoko Nakamura, Akio Kishida
Cancer treatment can be classified into surgical treatment, chemotherapy, radiotherapy, and immunotherapy. Cancer immunotherapy is a method for treating cancer using the immune system. To date, various cancer immunotherapies have been proposed, including vaccine therapy using autologous cancer vaccines [1], dendritic cell vaccines [2], and adoptive immunotherapy using natural killer (NK) cells and cytotoxic T cells [3]. Among these approaches, cancer immunotherapy related to regulatory T cells (Tregs) has recently become a major research focus. Tregs, i.e., CD4-, CD25-, and FoxP3-positive T cells, are key players in immune suppression [4] and function by controlling the activation of antigen-presenting cells via cytotoxic T lymphocyte antigen (CTLA)-4 and immunosuppressive cytokines (e.g., interleukin-10). In addition, Tregs play roles in suppressing the attack of T cells and other immune cells by modulating the production of transforming growth factor-β [5]. Furthermore, in the tumor microenvironment, which is formed by various components, including cancer cells, immune cells, and the extracellular matrix, Treg accumulation is induced by secretion of the chemokine C-C motif chemokine ligand 22 (CCL22) from cancer cells and tumor-infiltrating macrophages, resulting in an antitumor immune response [6,7]. Several treatments that inhibit immunosuppressive signal transduction by immune checkpoint inhibitors (e.g., anti-CTLA-4 and anti-programmed death-1 antibodies) and depletion of Tregs by administration of anti-C-C motif chemokine receptor 4 antibodies have been proposed as Treg-related cancer immunotherapies [8,9]. The development of selective Treg removal methods is also proposed [10,11]. Although the efficacies of these treatments have been demonstrated, treatment with immune checkpoint inhibitors can induce serious side effects owing to activation of T cells [12]. In addition, because Tregs are strongly related to autoimmunity, Treg-removing treatments may cause systemic autoimmune diseases. Therefore, the development of a method for local Treg removal at the tumor is essential.