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Details for anatomical structure: T-lymphocyte

EndoNet ID: ENC00287

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Synonyms

T-lymphocyte, T-cell, thymus-dependent lymphocyte, Lymphocytus

General information

they develop and mature in the thymus; major function is immune surveillance; they are activated by antigen-presenting cells and react either directly (via cytotoxic T-cells) or indirectly (via helper T-cells, which activate macrophages); they destroy e.g. virus-infected cells, bacterial infected cells; regulatory T-cells regulate or limit immune responses (suppressor T-cells)

Links to other resources

Cytomer cy0011313

Larger structures

    Substructures

      Secreted hormones

      • Hormone: SLAMF1 isoform 3

      • Hormone: IL-2

      • Hormone: IL-8

      • Hormone: IL-3

        • Hematopoietic cytokines such as interleukin 3 (IL-3) and granulocyte-macrophage colony stimulating factor (GM-CSF), produced by activated T cells and mast cells, are potent growth factors for various hematopoietic cells, as well as immature multipotential hematopoietic progenitors. [1]
      • Hormone: GM-CSF

        • Hematopoietic cytokines such as IL-3 and GM-CSF, produced by activated T cells and mast cells, are potent growth factors for various hematopoietic cells, as well as immature multipotential hematopoietic progenitors. [1]
      • Hormone: IL-4

        • IL-4-secreting CD4+ T cells are crucial to the development of CD8+ T-cell responses against malaria liver stages. [2]
      • Hormone: IL-5

      • Hormone: interleukin 6

      • Hormone: IL-9

      • Hormone: IL-10

      • Hormone: IL-13

        • Interleukin 13 is a T-cell-derived cytokine that regulates human monocyte and B-cell function. [3]
      • Hormone: IL-14

      • Hormone: IL-16

        • (CD8+)-T-lymphocytes.
      • Hormone: IL-17A

      • Hormone: TNF-beta

      • Hormone: IFN-gamma

        • In synergy with IFN-alpha or IL-12, IL-18 induces IFN-gamma production in T cells and enhances Th1 cell development. [4]

        Influenced by:

        • IL-18R
          in T-lymphocyte
      • Hormone: eotaxin-2

      • Hormone: osteopontin

      • Hormone: thymosin beta-4

      • Hormone: BAFF

      • Hormone: CXCL16

      • Hormone: fas Ligand

      • Hormone: IL-12B

      • Hormone: IL-17B

      • Hormone: IL-17E

      • Hormone: IL-32

      • Hormone: lymphotactin

      • Hormone: MIP-1 alpha

      • Hormone: MIP-1 beta

        • Perforin-low memory CD8+ cells are the predominant T cells in normal humans that synthesize MIP-1 beta. [5]
      • Hormone: PD-L1

      • Hormone: RANKL

        • Activated T cells can directly trigger osteoclastogenesis through OPGL (RANKL). Systemic activation of T cells in vivo leads to an OPGL-mediated increase in osteoclastogenesis and bone loss. [6]
      • Hormone: fibronectin

      • Hormone: oncostatin M

      • Hormone: IL-22

      • Hormone: FGF-1 isoform 1

      • Hormone: FGF-2

      • Hormone: CD5L

      • Hormone: natural soluble CD5 form

      • Hormone: soluble P-selectin

      • Hormone: SEMA4D

        • The generation of soluble CD100/Sema4D appears to be well regulated; its release from primary T cells is strictly dependent on a proteolytic cascade that follows cellular activation [7]

      Receptors

      • Receptor: leukosialin

      • Receptor: IL-18Rbeta

      • Receptor: IL-4Ralpha

      • Receptor: IL-10R-alpha

      • Receptor: IL-2R (low affinity)

      • Receptor: CCR4

      • Receptor: CCR7

      • Receptor: CD2

      • Receptor: H1

      • Receptor: H2

      • Receptor: IL-2R beta

      • Receptor: IL-2R gamma chain

      • Receptor: TLR1

      • Receptor: histamine H4 receptor

      • Receptor: leptin receptor

        Induced phenotype:

        • positive regulation of T cell activation
          • Leptin promotes lymphocyte survival in vitro by suppressing Fas-mediated apoptosis. [8]
          • Leptin binding to ObR results in increased STAT-3 activation in T cells [8]
      • Receptor: PPARgamma1

        • The peroxisome proliferation-activated receptor gamma (PPAR╬│)1 is a member of the nuclear receptor superfamily. It is expressed in many cell types, including adipocytes, epithelial cells, B- and T-cells, macrophages, endothelial cells, neutrophils, and smooth muscle cells [9]
      • Receptor: IL-18R1

      • Receptor: LIR-1

      • Receptor: CD7

      • Receptor: IL-18R

        Influences:

        • IFN-gamma
      • Receptor: ADAM17

        Induced phenotype:

        • ectodomain shedding
          • ADAM17 deficient lymphocytes failed to shed L-selectin in response to PMA. [10]
      • Receptor: CD6

      • Receptor: CD5

      • Receptor: SLAMF1 long form

      • Receptor: complement C3d receptor

      • Receptor: TCCR

      • Receptor: SIGLEC-7

      • Receptor: ALCAM

      • Receptor: hLAIR1-1

      • Receptor: PRLR

        Induced phenotype:

        • regulation of immune system process
          • Administration of PRL is also associated with an increase in T cell engraftment. [11]
      • Receptor: Sphingosine 1-phosphate receptor 1

        Induced phenotype:

        • cell maturation
          • Upregulation of S1PR1 expression or increased S1PR1 signalling suppresses the proliferation and maturation of mouse T cells. [12]
        • negative regulation of interferon-gamma production
          • In CD4+T cells, signalling through S1PR1 inhibits IFNgamma production, when compared with IL-4 production. [12]
        • positive regulation of interleukin-4 production
          • In CD4+T cells, signalling through S1PR1 increases IL-4 production. [13]
        • regulation of T cell proliferation
          • S1PR1 might modulate the proliferation of T cells. [14]
        • T cell differentiation during immune response
          • S1PR1 might decrease TH1-cell responses in vivo. [14]
          • S1PR1 might increase TH2-cell responses. [14]
          • S1PR1 might polarize TCR-activated cells towards a T helper 17-cell phenotype, thereby altering the immune response. [14]
          • S1P seems to increase the size of the TH17-cell subset through S1PR1 triggering. [15]
        • positive regulation of leukocyte migration
          • S1P has been reported to stimulate migration of T cells that express s1p1 under some conditions. T cell receptor-mediated activation of T cells suppresses expression of s1p1, and it has been reported to eliminate their migration responses to S1P. [16]
        • regulation of leukocyte migration
          • S1P signalling has a role in both the homing of immune cells to lymphoid organs, and in controlling their egress into blood and lymph. [17]
          • S1PR1 is decisive for T-cell egress from lymph nodes. [18]
      • Receptor: Sphingosine 1-phosphate receptor 4

        Induced phenotype:

        • negative regulation of interferon-gamma and interleukin-4 production
          • Signalling through S1PR4 in CD4+ T cells suppresses production of both cytokines, IFNgamma and IL-4, equally. [15]
        • positive regulation of interleukin-10 production
          • Signalling through S1PR4 in CD4+ T cells induces the production of IL-10. [15]
        • positive regulation of leukocyte migration
          • S1P has been reported to stimulate migration of T cells that express s1p4 under some conditions. T cell receptor-mediated activation of T cells suppresses expression of s1p4, and it has been reported to eliminate their migration responses to S1P. [16]
      • Receptor: Sphingosine 1-phosphate receptor 2

        Induced phenotype:

        • negative regulation of T cell apoptosis
          • Protection of T lymphocytes from apoptosis by S1P was associated with suppression of Bax expression via an EDG5- and EDG3-dependent mechanism. [19]
      • Receptor: Sphingosine 1-phosphate receptor 3

        Induced phenotype:

        • negative regulation of T cell apoptosis
          • Protection of T lymphocytes from apoptosis by S1P was associated with suppression of Bax expression via an EDG5- and EDG3-dependent mechanism. [19]
      • Receptor: Lysophosphatidic acid receptor 1

        Induced phenotype:

        • regulation of T cell chemotaxis
          • In activated T cells where LPA2 is downregulated while LPA1 is upregulated, LPA inhibits chemotaxis through LPA1. [20]
        • positive regulation of interleukin-2 production
          • In activated T cells where LPA2 is downregulated while LPA1 is upregulated, LPA activates IL-2 production through LPA1. [20]
        • positive regulation of interleukin-13 production
          • In activated T cells where LPA2 is downregulated while LPA1 is upregulated, LPA upregulates IL-13 through LPA1. [21]
        • positive regulation of activated T cell proliferation
          • In activated T cells where LPA2 is downregulated while LPA1 is upregulated, LPA activates cell proliferation through LPA1. [20]
      • Receptor: Lysophosphatidic acid receptor 2

        Induced phenotype:

        • negative regulation of interleukin-2 production
          • LPA inhibits interleukin-2 (IL-2) production in unstimulated T cells that predominantly express LPA2. [20]
        • regulation of T cell chemotaxis
          • LPA enhances chemotaxis in unstimulated T cells that predominantly express LPA2. [22]
      • Receptor: Probable G-protein coupled receptor 132

        Induced phenotype:

        • Systemic lupus erythematosus
          • Further complexity is introduced by the broad cellular involvement in SLE and the presence of related LPC receptors in multiple immune cell types. [23]
          • Several studies suggest that endogenously produced LPC may influence T cell responses and that receptor-mediated signals are involved. [23]
          • Increased levels of antibodies against LPC in patients with Systemic Lupus Erythematosus and the development of systemic autoimmune disease in G2A-deficient animals suggest a pathophysiological connection. How the pathology of this disease could relate to this receptor/ligand pair is likely to be complex considering the multiple susceptibility factors involved in SLE. [23]
        • modulation of T cell response
          • Genetic ablation of G2A function in mice has revealed a role for G2A in the homeostatic regulation of lymphocyte pools and the maintenance of immunological tolerance. G2A-deficient mice T lymphocytes exhibit hyperproliferative responses to antigen receptor stimulation. [24]
        • regulation of T cell activation
          • APC/T lymphocyte interactions within lymph nodes may be modulated by autocrine/paracrine production of LPC through G2A to influence the threshold for T cell activation. [23]
      • Receptor: Psychosine receptor

        Induced phenotype:

        • positive regulation of activation-induced cell death of T cells
          • The tissue-specific expression of TDAG8 and the induction of its expression during cell death of T cells mediated by the TCR or glucocorticoids suggest that it may have a role in activation-induced cell death of T cells. [25]
        • positive regulation of T cell differentiation in the thymus
          • The tissue-specific expression of TDAG8 and the induction of its expression during cell death of T cells mediated by the TCR or glucocorticoids suggest that it may have a role in activation-induced differentiation of T cells. [25]
      • Receptor: FTS receptor

        Induced phenotype:

        • positive regulation of T cell differentiation
          • Thymulin shows a large variety of effects on T cell functions, especially on T cell maturation. [26]
        • regulation of gene expression
          • In vivo thymulin treatment has effect on the IL-2R expression and on the avian CD4+ and CD8+ T cell populations. [27]
      • Receptor: IL-2R

        • Il-2 (...) binds to a high affinity receptor(..) found on Treg (regulatory T cell) cells and recently antigen-activated T-Lymphocytes [28]
      • Receptor: OX40

        • OX40 has since been characterized in mouse and human, where its expression is also restricted to activated T cells [29]
      Reference