Regulatory role of interleukin 2 and interleukin 4 in tumor regression of a mouse T-lymphoma

1995 ◽  
Vol 121 (S1) ◽  
pp. A21-A21
Author(s):  
K. Jurianz ◽  
P. von Hoegen
Keyword(s):  
Tumor Regression ◽  
Interleukin 2 ◽  
Regulatory Role ◽  
Interleukin 4 ◽  
T Lymphoma

scholarly journals Tumor regression by anti-CD40 and interleukin-2: role of CD40 in hematopoietic cells and organ-specific effects

2004 ◽  
Vol 10 (8) ◽  
pp. 534-539 ◽  
Author(s):  
Lisbeth A. Welniak ◽  
Lynnette Shorts ◽  
Jeff Subleski ◽  
Bruce R. Blazar ◽  
Robert H. Wiltrout ◽  
...  
Keyword(s):  
Tumor Regression ◽  
Interleukin 2 ◽  
Hematopoietic Cells ◽  
Specific Effects ◽  
Organ Specific

Functional Role of Interleukin-4 (IL-4) and IL-7 in the Development of X-Linked Severe Combined Immunodeficiency

Blood ◽  
1999 ◽  
Vol 93 (2) ◽  
pp. 607-612 ◽  
Author(s):  
Satoru Kumaki ◽  
Naoto Ishii ◽  
Masayoshi Minegishi ◽  
Shigeru Tsuchiya ◽  
David Cosman ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Severe Combined Immunodeficiency ◽  
T Cell Development ◽  
Interleukin 2 ◽  
Cell Development ◽  
Interleukin 4 ◽  
Combined Immunodeficiency ◽  
Survival Signal

X-linked severe combined immunodeficiency (X-SCID) is characterized by an absent or diminished number of T cells and natural-killer (NK) cells with a normal or elevated number of B cells, and results from mutations of the γc chain. The γc chain is shared by interleukin-2 (IL-2), IL-4, IL-7, IL-9, and IL-15 receptors. Recently, a survival signal through the IL-7 receptor  (IL-7R) chain was shown to be important for T-cell development in mice and was suggested to contribute to the X-SCID phenotype. In the present study, we examined function of a mutant γc chain (A156V) isolated from an X-SCID patient and found that T cells expressing the mutant γc chain were selectively impaired in their responses to IL-4 or IL-7 compared with the wild-type γc chain expressing cells although responses to IL-2 or IL-15 were relatively maintained. The result shows that IL-4– and/or IL-7–induced signaling through the γc chain is critical for T-cell development and plays an important role in the development of the X-SCID phenotype.

Apoptosis following interleukin-2-withdraw from T cells: Evidence for a regulatory role of CD18 (β2-integrin) molecules

1997 ◽  
Vol 56 ◽  
pp. 68-69
Author(s):  
Anders Woetmann ◽  
Paul Gladstone ◽  
Jeffrey A. Ledbetter ◽  
Arne Svejgaard ◽  
Niels Ødum ◽  
...  
Keyword(s):  
T Cells ◽  
Interleukin 2 ◽  
Regulatory Role ◽  
Β2 Integrin

scholarly journals In vivo role of interleukin 4 in T cell tolerance induced by aqueous protein antigen.

1993 ◽  
Vol 177 (2) ◽  
pp. 457-463 ◽  
Author(s):  
H J Burstein ◽  
A K Abbas
Keyword(s):  
T Cells ◽  
T Cell ◽  
Interleukin 2 ◽  
Interleukin 4 ◽  
Th2 Cells ◽  
High Dose ◽  
Protein Antigens ◽  
Ifn Gamma

High doses of aqueous protein antigens induce a form of immunological tolerance in which interleukin 2 (IL-2)- and interferon gamma (IFN-gamma)-secreting T helper type 1 (Th1) cells are inhibited, but IL-4-secreting (Th2) cells are not. This is manifested by reduced proliferation of antigen-specific T cells upon in vitro restimulation, and marked suppression of specific antibody responses of the immunoglobulin (Ig)G2a, IgG2b, and IgG3 isotypes, but not of IgG1 and IgE. The role of the immunomodulatory cytokine IL-4 in this model of unresponsiveness to protein antigens has been examined. Administration of tolerizing antigen itself primes splenic CD4+ T cells for secretion of lymphokines, both IL-2 and IL-4. Neutralization of IL-4 in vivo with the anti-IL-4 antibody 11B11 during tolerance induction augments IFN-gamma production by T cells of tolerant mice, and reverses the suppression of IgG2a, IgG2b, and IgG3. This blockade of IL-4 function does not, however, restore the proliferative responses of T cells, suggesting that reduced T cell proliferation is due to direct T cell inactivation or anergy. Inhibiting the activity of IL-4 in vivo also inhibits the expansion of antigen-specific Th2-like cells, which are resistant to the induction of unresponsiveness. Thus, the immunologic consequences of high-dose tolerance are due to a combination of clonal T cell anergy and IL-4-mediated immune regulation.

JAB/SOCS1/SSI-1 is an interleukin-2–induced inhibitor of IL-2 signaling

Blood ◽  
2001 ◽  
Vol 97 (1) ◽  
pp. 221-226 ◽  
Author(s):  
Bernhard Sporri ◽  
Panu E. Kovanen ◽  
Atsuo Sasaki ◽  
Akihiko Yoshimura ◽  
Warren J. Leonard
Keyword(s):  
Kinase Activity ◽  
Interleukin 2 ◽  
Sh2 Domain ◽  
Interleukin 4 ◽  
Cytokine Signaling ◽  
Suppressor Of Cytokine Signaling ◽  
Cell Responses ◽  
Ifn Γ ◽  
Induced Signal

Abstract JAB/suppressor of cytokine signaling 1 (SOCS1) STAT-induced STAT inhibitor–1 (SSI-1) (JAB/SOCS1/SSI-1) is an SH2-domain–containing protein that is induced by and negatively regulates signaling by a number of cytokines including interleukin-4 (IL-4), IL-6, interferon (IFN)-γ, prolactin, growth hormone, and erythropoietin. The role of JAB/SOCS1/SSI-1 in IL-2 signaling has been analyzed. JAB/SOCS1/SSI-1 is strongly induced by IL-2 in peripheral blood T cells, and JAB/SOCS1/SSI-1 overexpression strongly inhibits IL-2–induced signal transducer and activator of transcription–5 (Stat5) phosphorylation and transcriptional activity. In cotransfection experiments, JAB/SOCS1/SSI-1 associates with both Jak1 and Jak3; however, JAB/SOCS1/SSI-1 had a greater effect on Jak1 tyrosine phosphorylation and kinase activity. JAB/SOCS1/SSI-1 also interacts with IL-2Rβ, and this interaction requires the A region (residues 313-382) of IL-2Rβ. However, this interaction was not essential for the inhibitory action of JAB. Thus, JAB/SOCS1/SSI-1 is an IL-2–induced inhibitor of IL-2 signaling that functions by inhibiting Jak kinase activity. This suggests an important role for JAB/SOCS1/SSI-1 in regulating T-cell responses.

Functional Role of Interleukin-4 (IL-4) and IL-7 in the Development of X-Linked Severe Combined Immunodeficiency

Blood ◽  
1999 ◽  
Vol 93 (2) ◽  
pp. 607-612 ◽  
Author(s):  
Satoru Kumaki ◽  
Naoto Ishii ◽  
Masayoshi Minegishi ◽  
Shigeru Tsuchiya ◽  
David Cosman ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Severe Combined Immunodeficiency ◽  
T Cell Development ◽  
Interleukin 2 ◽  
Cell Development ◽  
Interleukin 4 ◽  
Combined Immunodeficiency ◽  
Survival Signal

Abstract X-linked severe combined immunodeficiency (X-SCID) is characterized by an absent or diminished number of T cells and natural-killer (NK) cells with a normal or elevated number of B cells, and results from mutations of the γc chain. The γc chain is shared by interleukin-2 (IL-2), IL-4, IL-7, IL-9, and IL-15 receptors. Recently, a survival signal through the IL-7 receptor  (IL-7R) chain was shown to be important for T-cell development in mice and was suggested to contribute to the X-SCID phenotype. In the present study, we examined function of a mutant γc chain (A156V) isolated from an X-SCID patient and found that T cells expressing the mutant γc chain were selectively impaired in their responses to IL-4 or IL-7 compared with the wild-type γc chain expressing cells although responses to IL-2 or IL-15 were relatively maintained. The result shows that IL-4– and/or IL-7–induced signaling through the γc chain is critical for T-cell development and plays an important role in the development of the X-SCID phenotype.

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