Effects of substance P on human T cell function and the modulatory role of peptidase inhibitors

Covas, M. J.; Pinto, Lígia A.; Victorino, Rui M. M.

doi:10.1007/bf02912447

Cited by 8 publications

(6 citation statements)

References 34 publications

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“…Nevertheless, the amino-terminal penultimate proline is resistant to cleavage by other aminopeptidases, lending protection against degradation. Consequently, removal of the amino-terminal dipeptide by DPPIV significantly shortens the in vivo biological half-life of SP [ 74 ].…”

Section: The Dash Family Substrates: Enzymatic Regulation and Their Rmentioning

confidence: 99%

Untitled

et al. 2005

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253 ADA = adenosine deaminase; CCL = CC ligand; CCR = CC receptor; CGRP = calcitonin gene-related peptide; CXCL = CXC ligand; CXCR = CXC receptor; DASH = dipeptidyl peptidase-IV activity and/or structure homologues; DPP = dipeptidyl peptidase; FAP-α = fibroblast-activation protein α/seprase; GLP-1 = glucagon-like peptide-1; GRP = gastrin releasing peptide; HLA = human leukocyte antigens; IFN = interferon; IL = interleukin; IP-10 = IFN-γ inducible protein-10; Mig = monokine induced by interferon-γ; MIP = macrophage inflammatory protein; NAALADase = N-acetylated α-linked acidic dipeptidase; NK = natural killer; NPY = neuropeptide Y; OA = osteoarthritis; PB = peripheral blood; QPP = quiescent cell proline dipeptidase; RA = rheumatiod arthritis; RANTES = regulated upon activation normal T-cell expressed and secreted; SDF = stromal cellderived factor; SF = synovial fluid; SLE = systemic lupus erythematosus; SP = substance P; TGF = transforming growth factor; TNF = tumor necrosis factor; VIP = vasoactive intestinal peptide. Available online http://arthritis-research.com/content/7/6/253 AbstractSeveral of the proinflammatory peptides involved in rheumatoid arthritis pathogenesis, including peptides induced downstream of tumor necrosis factor-α as well as the monocyte/T cell-attracting chemokines RANTES and stromal cell-derived factor (SDF)-1α and the neuropeptides vasoactive intestinal peptide (VIP) and substance P, have their biological half-lives controlled by dipeptidyl peptidase IV (DPPIV). Proteolysis by DPPIV regulates not only the half-life but also receptor preference and downstream signaling. In this article, we examine the role of DPPIV homologs, including CD26, the canonical DPPIV, and their substrates in the pathogenesis of rheumatoid arthritis. The differing specific activities of the DPPIV family members and their differential inhibitor response provide new insights into therapeutic design.

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Section: The Dash Family Substrates: Enzymatic Regulation and Their Rmentioning

confidence: 99%

Untitled

et al. 2005

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“…Interestingly, T lymphocytes and monocytes bear specific receptors for this neuropeptide, mainly the neurokinin 1 (NK-1) receptor ( 96 , 98 ). Noteworthy, SP has been reported to modulate the phenotype and function of these cells ( 99 , 100 ). For example, peripheral blood human T cells stimulated with PHA plus PMA (T cell activators) in the presence of SP increased the expression of IL-2, a cytokine indicative of T cell activation ( 99 , 101 ).…”

Section: Neuronal Signals Regulating the Immune System And Hsv-1 Infectionmentioning

confidence: 99%

“…Noteworthy, SP has been reported to modulate the phenotype and function of these cells ( 99 , 100 ). For example, peripheral blood human T cells stimulated with PHA plus PMA (T cell activators) in the presence of SP increased the expression of IL-2, a cytokine indicative of T cell activation ( 99 , 101 ). Moreover, SP also increased the production of IL-17A and IFN-γ by human memory CD4 + T cells, which favored their polarization towards a Th17/Th1 profile that was dependent of monocyte-derived proinflammatory cytokines ( 102 ).…”

Section: Neuronal Signals Regulating the Immune System And Hsv-1 Infectionmentioning

confidence: 99%

Crosstalk Between Epithelial Cells, Neurons and Immune Mediators in HSV-1 Skin Infection

et al. 2021

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Herpes simplex virus type 1 (HSV-1) infection is highly prevalent in humans, with approximately two-thirds of the world population living with this virus. However, only a fraction of those carrying HSV-1, which elicits lifelong infections, are symptomatic. HSV-1 mainly causes lesions in the skin and mucosae but reaches the termini of sensory neurons innervating these tissues and travels in a retrograde manner to the neuron cell body where it establishes persistent infection and remains in a latent state until reactivated by different stimuli. When productive reactivations occur, the virus travels back along axons to the primary infection site, where new rounds of replication are initiated in the skin, in recurrent or secondary infections. During this process, new neuron infections occur. Noteworthy, the mechanisms underlying viral reactivations and the exit of latency are somewhat poorly understood and may be regulated by a crosstalk between the infected neurons and components of the immune system. Here, we review and discuss the immune responses that occur at the skin during primary and recurrent infections by HSV-1, as well as at the interphase of latently-infected neurons. Moreover, we discuss the implications of neuronal signals over the priming and migration of immune cells in the context of HSV-1 infection.

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“…Together, these results show that the positive and negative effects of peptides derived from the PPT-I gene are complex and include other genes that might be regulated by the tachykinin family of peptides. 39 When the conventions of head (residues 1-4) and tail (residues 5-11) are used for SP, certain assumptions can be made about the structure of SP. The model, shown in Figure 8A, indicates no helical structure of SP but a curve in the head region.…”

Section: Discussionmentioning

confidence: 99%