Interferon: a cytotoxic T lymphocyte differentiation signal

Chen, Likuang; Tourvieille, B.; Burns, Gordon F.; Bach, Fritz H.; Mathieu-Mahul, D.; Sasportes, M; Bensussan, Armand

doi:10.1002/eji.1830160709

Cited by 108 publications

(30 citation statements)

References 22 publications

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“…Serum IFN-γ concentration was also observed to have increased simultaneously. Administration of activated CD4 + cells and CD8 + cells would promote the secretion of IL-2 and IFN-γ, thus inducing proliferation and activation of T and NK cells, and further accelerating IFN-γ production [6,7]. Serum IFN-γ concentration was increased first, and then, the cytotoxic ability of the PBMCs might be have been enhanced, since IFN-γ promoted the activation of NK cells [35].…”

Section: Discussionmentioning

confidence: 99%

Phenotypic Analysis and Effects of Sequential Administration of Activated Canine Lymphocytes on Healthy Beagles

et al. 2008

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ABSTRACT. We attempted to accumulate the basic data for evaluation of activated lymphocyte therapy for small animal medicine. The peripheral blood mononuclear cells (PBMCs) collected from healthy dogs were activated using anti-CD3 antibody and human recombinant (hr) interleukin (IL)-2 and reactivated using hr interferon (IFN)-α and hr IL-2. The property of obtained cells was compared with PBMCs. The number of cells was shown to have increased approximately > 50 -fold by cultivation. The proportion of CD8 + cells was significantly increased, the cytotoxicity of the cultured cells was revealed to have been reinforced. Additionally, CD56 mRNA levels tended to have increased. The cells obtained by this method were confirmed to be activated lymphocytes. Furthermore, we investigated the effects of sequential administration of the obtained cells to healthy dogs. By sequential administration of the activated lymphocytes, the cell proliferative activity, proportion of CD4 + cells and CD8 + cells, and serum IFN-γ concentration were shown to have increased, and no severe adverse effects were observed. Consequently, activated lymphocytes could be induced using anti-CD3 antibody and IL-2 in healthy dogs, and sequential administration of activated lymphocytes reinforced the recipient's immunity.

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Section: Discussionmentioning

confidence: 99%

Phenotypic Analysis and Effects of Sequential Administration of Activated Canine Lymphocytes on Healthy Beagles

et al. 2008

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“…This cytokine has been known to these two cytokines to almost equal extents should be considered. The first possibility is that although hepaactivate macrophages, 21 to enhance differentiation of cytotoxic T lymphocytes, 22,23 and to increase antigen-tocellular damage is induced mainly by one cytokine, the production of this cytokine requires the participapresenting capability by upregulating the expression of major histocompatibility complex antigens. 24,25 IFN-tion of the other alternative cytokine.…”

Section: Infiltration Of Blastoid T Cells In the Liver From Micementioning

confidence: 99%

Critical Involvement of Interferon γ in the Pathogenesis of T–Cell Activation–Associated Hepatitis and Regulatory Mechanisms of Interleukin–6 for the Manifestations of Hepatitis

et al. 1996

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Liver disease, including hepatitis and cirrhosis, repmodel. Striking increases in the plasma levels of various resent a major cause of morbidity and mortality. In cytokines, including tumor necrosis factor (TNF), in-chronic hepatitis, liver parenchymal cells are destroyed terleukin-2 (IL-2), and IFN-g, were detected before the by host lymphoid cells, especially by activated T cells increase in plasma aminotransferase levels induced by responding to viral antigens. 1 The cellular and molecuCon A injection. TNF levels peaked within 2 hours, lar mechanisms underlying the development of hepatowhereas IFN-g levels peaked at 6 hours after Con A injeccellular destruction have not been studied extensively tion. In contrast to a sharp peak of TNF levels, high IFNg levels were detected for a more prolonged period. because of the lack of availability of suitable animal Passive immunization with anti-IFN-g monoclonal anti-models. body (MAb) conferred a dose-dependent protectionRecently, a new hepatitis model was developed in against liver injury in this model. This protection was which liver-specific inflammatory lesions are induced observed when anti-IFN-g MAb was administered at by injection of concanavalin A (Con A). 2 Importantly, least 30 minutes before Con A injection but not when the hepatitis could be induced without pretreatment given 1 hour after Con A injection. The protection from with D-galactosamine, 3 which is an absolute requireCon A-induced hepatitis was also induced by adminis-ment for the induction of hepatitis by injection of endotration of rIL-6 before Con A injection. rIL-6 treatment toxin from gram-negative bacteria such as lipopolysacinduced significant albeit incomplete inhibition of IFNcharide (LPS). 4,5 Furthermore, the hepatic injury g and TNF production, whereas this regimen did not affect IL-2 production. Despite striking protective ef-appears to be a consequence of T-cell activation. 2,6 Our fects of rIL-6 or anti-IFN-g MAb, comparable levels of initial study 6 using this model showed that tumor necellular (both T cell and polymorphonuclear cell) infil-crosis factor (TNF) and interleukin-6 (IL-6) function as tration were detected in liver sections from animals un-positive and negative modulators, respectively, for the treated, or treated with either rIL-6 or anti-IFN-g MAb. development of Con A-induced hepatitis. Despite the Moreover, electron microscopic examination showed massive production of interferon gamma (IFN-g) by that infiltrating T cells exhibited a blastoid appearance Con A-stimulated T cells in vitro, the involvement of in all groups. These results indicate that IFN-g plays a this cytokine in the pathogenesis in Con A-induced critical role in the development of Con A-induced acute hepatitis has not been investigated. It is increasingly hepatitis and suggest that IL-6 administration can reguevident that IFN-g produced by T cells after stimula-

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“…A monoclonal antibody (mAb) termed Leo A1 and F(ab 1 ) 2 fragments of this mAb and of a polyclonal antibody to TLiSA1 inhibited the differentiation of human pCTL into effector cells when present during mixed lymphocyte culture but had no effect on cell proliferation or cytolytic function (7,8). The mAb also inhibited the interferon-induced differentiation of human pCTL clones into cytotoxic effector cells, an effect that did not involve blocking of interferon binding (9).…”

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confidence: 90%

TLiSA1 (PTA1) Activation Antigen Implicated in T Cell Differentiation and Platelet Activation Is a Member of the Immunoglobulin Superfamily Exhibiting Distinctive Regulation of Expression

Sherrington¹,

Scott²,

Jin³

et al. 1997

Journal of Biological Chemistry

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T lineage-specific activation antigen 1 (TLiSA1) antigen was initially described as a T lineage-specific activation antigen involved in the differentiation of human cytotoxic T cells. Subsequently, the antigen was identified on platelets and was shown to be involved in platelet activation, hence it was renamed platelet and T cell antigen 1 (PTA1), although identity between the two antigens was not established. In the present study we have cloned the cDNA encoding TLiSA1 from Jurkat cells and show it to be a novel member of the immunoglobulin superfamily with the unusual structure of two V domains only. Identity between TLiSA1 and platelet PTA1 is established by immunological criteria, by internal peptide sequences obtained from the purified platelet glycoprotein and by sequencing the platelet transcript after reverse transcriptase-polymerase chain reaction. In Jurkat cells, TLiSA1/PTA1 mRNA and surface protein expression is greatly stimulated by treatment of the cells with phorbol ester, but the T cell proliferative signal of phorbol ester and ionophore combined greatly reduces or abrogates this response, and this suppressive effect of the ionophore is not reversed by incorporating FK506 to inhibit calcineurin. Together with the known signaling role of PTA1, these data substantiate the notion that this molecule is implicated in T cell differentiation, perhaps by engagement of an adhesive ligand.

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Interferon: a cytotoxic T lymphocyte differentiation signal

Cited by 108 publications

References 22 publications

Phenotypic Analysis and Effects of Sequential Administration of Activated Canine Lymphocytes on Healthy Beagles

Phenotypic Analysis and Effects of Sequential Administration of Activated Canine Lymphocytes on Healthy Beagles

Critical Involvement of Interferon γ in the Pathogenesis of T–Cell Activation–Associated Hepatitis and Regulatory Mechanisms of Interleukin–6 for the Manifestations of Hepatitis

TLiSA1 (PTA1) Activation Antigen Implicated in T Cell Differentiation and Platelet Activation Is a Member of the Immunoglobulin Superfamily Exhibiting Distinctive Regulation of Expression

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