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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

  • circulatory_system__hematopoietic_system
  • parts_of_human_body
  • thymus
  • immune_system
  • blood
  • spleen

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 (PPARÎł)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