Studies on T lymphocyte activation I. Requirements for the mitogen‐dependent production of T cell growth factors

Andersson, Jan; Grönvik, Kjell-Olov; Larsson, Eva‐Lotta; Coutinho, António

doi:10.1002/eji.1830090802

Cited by 130 publications

(33 citation statements)

References 27 publications

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“…ConA activation of T cells is an APC-dependent process (24). A difference in the induced cytokine profile was seen when CD4 T cells (including iNKT cells) were cocultured with CD4…”

Section: Discussionmentioning

confidence: 99%

IL-22-Dependent Attenuation of T Cell-Dependent (ConA) Hepatitis in Herpes Virus Entry Mediator Deficiency

Wahl¹,

Wegenka²,

Leithäuser

et al. 2009

The Journal of Immunology

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Coinhibitors and costimulators control intrahepatic T cell responses that trigger acute hepatitis. We used the ConA-induced hepatitis model in the mouse to test if the coinhibitor herpes virus entry mediator (HVEM) modulates hepatitis-inducing T cell responses. Compared with ConA-injected, wild-type (wt) C57BL/6 (B6) mice, HVEM-deficient (HVEM−/−) B6 mice showed lower serum transaminase levels and lower proinflammatory IFN-γ, but higher protective IL-22 serum levels and an attenuated liver histopathology. The liver type I invariant NKT cell population that initiates acute hepatitis in this model was reduced in HVEM−/− mice but their surface phenotype was similar to that of untreated or ConA-treated wt controls. In response to mitogen injection, liver invariant NKT cells from HVEM−/− B6 mice produced in vivo more IL-22 but lower amounts of IFN-γ and IL-4 than wt controls. Bone marrow chimeras showed that HVEM deficiency of the liver nonparenchymal cell population, but not of the parenchymal cell population, mediated the attenuated course of the dendritic cell- and T cell-dependent ConA hepatitis. IL-22 is produced more efficiently by liver NKT cells from HVEM−/− than from wt mice, and its Ab-mediated neutralization of IL-22 aggravated the course of hepatitis in wt and HVEM−/− mice. Hence, HVEM expression promotes pathogenic, proinflammatory Th1 responses but down-modulates protective IL-22 responses of T cells in this model of acute hepatitis.

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“…ConA activation of T cells is an APC-dependent process (24). A difference in the induced cytokine profile was seen when CD4 T cells (including iNKT cells) were cocultured with CD4…”

Section: Discussionmentioning

confidence: 99%

IL-22-Dependent Attenuation of T Cell-Dependent (ConA) Hepatitis in Herpes Virus Entry Mediator Deficiency

Wahl¹,

Wegenka²,

Leithäuser

et al. 2009

The Journal of Immunology

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“…The requirement for accessory cells appears to be limited to their participation in the production of TCGF [3,7,131 The responsiveness of activated T cells to growth factors appears to be the result of the expression of an acceptor site on the surface membrane which is not presented on resting cells, as determined by adsorption experiments [2, 31. To confirm this hypothesis, the demonstration that the "absorbed" TCGF can be eluted from the T blasts is still required.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of T cell activation I. A screening of “step one” ligands

Larsson¹,

Coutinho²

1980

Eur J Immunol

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A number of ligands which bind to T cell surfaces were screened on murine spleen cells for their functional ability to induce either of the two necessary steps in the process of T cell triggering: (a) expression of growth receptors by T lymphocytes and (b) production of T cell growth factors in cultures containing both T cells and accessory cells. Among four lectins tested, concanavalin A was found to induce both responses but is primarily a “step 2” ligand, in particular at low concentrations; leucoagglutinin was the most potent “step 1” ligand with very limited “step 2” activity; wheat germ agglutinin and soybean lectin were inactive. Direct mitogenicity of the lectin to normal spleen cell cultures was limited by the poorest of these two functional properties. A number of rabbit anti‐lymphocyte antisera, anti‐Thy‐1 alloantisera, anti‐H‐2 and anti‐Ia monoclonal antibodies, as well as complexes of rabbit IgG, were all found to be devoid of “step 1” activity, and consequently, non‐ mitogenic for spleen cells. In contrast, a rabbit anti‐mouse brain antiserum, although also devoid of mitogenicity, was found to be capable of “step 1” induction. These results suggest that not all rearrangements of T cell surface membrane components upon binding of a ligand result in the functional expression of growth receptors. This appears to be the result of selective interactions with specific sites which include structures binding to concanavalin A, leucoagglutinin and rabbit anti‐mouse brain antibodies.

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“…When lymphocytes are cultured beyond the proliferative peak in MLR and the peak in CTL activity (i.e. activated T cells), lymphocyte prolifera tion is strictly dependent on IL-2 [18][19][20]. SDIF inhi bits this IL-2-dependent proliferation, an excess of the interleukin being unable to restore the prolifera tive response of primed lymphocytes.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Cytotoxic T Lymphocytes by a Schistosome-Derived Inhibitory Factor Is Independent of an Inhibition of the Production of Interleukin 2

Mazingue¹,

Dessaint²,

Schmitt-Verhulst³

et al. 1983

Int Arch Allergy Immunol

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Schistosome-derived inhibitory factor (SDIF) was shown to inhibit lymphocyte proliferation. While SDIF is not toxic to lymphoid cells, the generation of cytotoxic effector cells was inhibited by SDIF in a mixed lymphocyte culture. This inhibitory effect was not attributable to the induction of suppressor cells, as SDIF also inhibited the development of nonspecific suppressor cell activity in 7-day cultures of unstimulated spleen cells. The interleukine 2-dependent proliferation of cytotoxic T lymphocytes of or of blast cells was markedly reduced by the addition of SDIF. In contrast, the production of interleukine 2 itself was not impaired by SDIF. These results support the hypothesis of an inhibition by SDIF of a particular step of the mitotic cycle, probably posterior to the G₀-G₁ transition. An inhibitory activity of SDIF on the expression of the cytolytic activity of cytotoxic T lymphocytes was also observed.

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Studies on T lymphocyte activation I. Requirements for the mitogen‐dependent production of T cell growth factors

Cited by 130 publications

References 27 publications

IL-22-Dependent Attenuation of T Cell-Dependent (ConA) Hepatitis in Herpes Virus Entry Mediator Deficiency

IL-22-Dependent Attenuation of T Cell-Dependent (ConA) Hepatitis in Herpes Virus Entry Mediator Deficiency

Mechanism of T cell activation I. A screening of “step one” ligands

Inhibition of Cytotoxic T Lymphocytes by a Schistosome-Derived Inhibitory Factor Is Independent of an Inhibition of the Production of Interleukin 2

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