Cytokines and Their Modifying Influences
المؤلف:
Hoffman, R., Benz, E. J., Silberstein, L. E., Heslop, H., Weitz, J., & Salama, M. E.
المصدر:
Hematology : Basic Principles and Practice
الجزء والصفحة:
8th E , P125-126
2025-10-20
73
Many CSFs have been implicated in the pathobiology of both hematopoietic and nonhematopoietic disorders or have been used after production by recombinant DNA technology to treat patients. Cytokines are involved in regulation of hematopoiesis at the level of HSC, HPC, and more mature blood or other accessory cells. Accessory cells include stromal cells (which are themselves very het erogenous), endothelial cells, cells belonging to lymphoid lineages (T cells, B cells, natural killer [NK] cells, NKT cells), and innate immune cells (monocytes/macrophages, neutrophilic myeloid cells, dendritic cells [DCs]). Cell regulation is not necessarily easily dissectible, but strides have been made in elucidating these intricate cytokine-cell interactions. Cytokine receptor signaling has been reviewed. Cytokines are involved in developmental processes during embryogenesis, through neonatal, and into adult life. They can fight infections and elicit immune responses. Redundancy in cytokine(s), their receptors, and actions are probably nature’s way to protect the body against unwanted insults that may interfere with specific cytokines and their protective actions. ILs and chemokines are part of the cytokine superfamily of molecules. ILs, chemokines, and their receptors are covered in this chapter, as will other bio logically active proteins that influence hematopoiesis. Cytokines are secreted by leukocytes, as well as other cells. They act on, but are not limited to, hematopoietic cells to regulate blood cell pro duction; this includes effects on immune cells and during inflammation. Biologically active proteins influence in vitro and in vivo proliferation, differentiation, and survival/apoptosis (programmed cell death) at the level of HSC, HPC, and more mature cells of the hematopoietic system. It is clear that activities of these proteins can be modified by enzymatic cleavage, such as that mediated by dipeptidylpeptidase (DPP) 4 (a.k.a. CD26), and also in context of oxygen tensions that are vastly different in vivo (~1% to 5% O2 in BM, and also low in blood and other tissues, from that of the ambient air conditions of ~21% O2 in which most investigators have studied the in vitro and ex vivo activities of these growth regulators). These potent cytokines/chemokines/other growth regulators and their receptors are discussed throughout the chapter. It is not possible to truly understand the action(s) of cytokines and other growth-modulating factors in absence of these modulating/modifying influences on cytokine activities.
Importantly, cytokine-cell interactions can become dysregulated and induce or be involved in pathologic situations. Examples of some adverse pathologic effects of cytokines include the “cytokine storm” elicited following chimeric antigen receptor (CAR) T-cell therapy, during inflammation, and after infection with viruses, such as SARS-CoV-2. Thus cytokine-cell interactions present a “double-edged sword” for both “good” (physiologic) and “bad” (pathologic) effects. Specific information on cytokines, chemokines, iron-binding proteins, other biologically active proteins, and growth regulation and their receptors follows.
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