CD8+ Suppressor T Cell Clone 13G2 Secretes a Suppressive Lymphokine, Immune Suppressive Factor-T (ISF-T)

Hisatsune, Tatsuhiro; Nishijima, Ken-ichi; Minai, Yuji; Enomoto, Atsushi; Kaminogawa, Shuichi

doi:10.1007/978-94-011-3550-4_3

Cited by 3 publications

(3 citation statements)

References 7 publications

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“…However, further studies have shown that human IL-10 is not only produced by typical Th2 cells, but also by Th0 cells, Th1 cells [21], Ts cells [22], Tr1 cells [23], B cells [24,25], monocytes [26], keratinocytes [27,28] and many tumor cells as well as cell lines [29][30][31].…”

Section: Brief Overview Of Il-10mentioning

confidence: 99%

Boosting Interleukin-10 Production: Therapeutic Effects and Mechanisms

Zhou¹,

Schmidtke²,

Zepp³

et al. 2005

curr drug targets immune endocr metabol disord

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More than forty cytokines have been extensively researched on the molecular structure, cell signaling and transduction pathway. With respect to cytokine-regulating therapy in immunological imbalance however, the reported results are conflicting because of the pleiotropic functions and the intricate interactions of the cytokine network. In this review, we outline the observations on interleukin-10 (IL-10) upregulatory therapy. Despite varying opinions on its therapeutic effects for different disorders, IL-10 has been considered a potential anti-inflammatory cytokine. Numerous studies support the view that IL-10 shows a strong suppressive effect on Th1 lymphocytes, antigen presenting cells and the production of inflammatory mediators. It is also noticeable that recent research has revealed the relationship between IL-10 induced antigen specific regulatory CD4+ T cells and antigen specific immune tolerance. This specific regulation was mediated in part through IL-10 secretion, because anti-IL-10 treatment reverted the inhibitory effect of regulatory T cell clones. In different models, these cells were shown to inhibit both Th1 and Th2-type inflammatory responses through the secretion of IL-10. With the presence of IL-10, regulatory T cells may induce peripheral immune tolerance. Exogenous administration, transgenic expression and endogenous stimulative agents of IL-10 have been used for a variety of inflammatory diseases, autoimmune diseases and allograft rejection in patients and experimental models. A therapeutic intervention with drug inducing endogenous IL-10 may be more practical than an exogenous administration of IL-10 with transient effect. Although further investigation on gene regulation of IL-10 is necessary, increasing studies have been reported concerning the attempt to develop the agents, which could promote endogenous IL-10 production for the treatment of immunological disorders and inflammatory diseases. With some unclear mechanisms, these agents have strongly upregulated IL-10 production in vitro or in vivo. Reported IL-10 upregulatory agents have shown promising prospects for remission of autoimmune diseases and inflammatory diseases and have even induced antigen specific immune tolerance. It is interesting that the IL-10 upregulatory effect of several traditional immunosuppressive drugs has been detected, e.g. glucocorticoid, which is considered "not more as an immunosuppressive drug but an immune modulating agent". Approximately twenty IL-10 upregulatory agents as instances are described in the present review. In addition, their therapeutic effects in various diseases are discussed.

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Section: Brief Overview Of Il-10mentioning

confidence: 99%

Boosting Interleukin-10 Production: Therapeutic Effects and Mechanisms

Zhou¹,

Schmidtke²,

Zepp³

et al. 2005

curr drug targets immune endocr metabol disord

View full text Add to dashboard Buy / Rent full text

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“…In chronic HVGD and GVHD models, an imbalance between Th2 and Thl cell subclasses has been described (reviewed in [43]). The excess and /or increased activity of Th2 cells might lead to the overproduction of inhibitory cytokines [44,45]. Inhibition of the mitogen receptors can also be assumed, e.g., by the autoimmune ATA present in most of the animals.…”

Section: Discussionmentioning

confidence: 99%

Autoimmunity, hyporeactivity to T cell mitogens and lymphoproliferative disorders following neonatal induction of transplantation tolerance in mice

et al. 1993

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We have reported that, in A/J (A) (H-2a) mice, a partial tolerance to C57BL/10ScSn (B10) (H-2b) skin allografts and a high incidence of lethal lymphoproliferative disorders (LPD) can be induced by the neonatal i.v. injection of 2 x 10(7) semiallogeneic (B10 x A)F1 spleen cells (SC) (Végh, P., Baranyi, L. and Jánossy, T., Cell. Immunol. 1990, 129: 56). In this study, we show that the incidence and mortality of LPD were continuously growing from 1 month of age until the end of the experiment at 1 year (64% and 36%, respectively). Based on histology, 27% of the diseased mice suffered from lymphoid malignancies. In the remaining cases (73%), reactive histopathological changes were seen in the spleen, lymph nodes (LN), liver and kidneys. The proportion of CD4+ T cells in the spleen and LN as well as that of splenic B cells decreased, while the percentages of mature and immature myeloid cells doubled. The total cell number of each (sub)population, however, was elevated in both lymphoid organs. The cells taking part in the lymphoproliferation were of host (A) and not of donor (F1) origin. Preceding the development of apparent LPD, the SC, LN cell and thymus cell suspensions of 1-month-old tolerized mice showed reduced in vitro proliferative responses to T cell and T cell-dependent B cell mitogens (Con A or PWM), while their reactivity to a T cell-independent B cell mitogen (lipopolysaccharide) was essentially unimpaired. This hyporeactivity seems to be functional, because neither histology nor immunophenotyping by flow cytometry revealed significant alterations in the spleen and thymus of such animals, apart from a slight reduction in the ratio of CD4+/CD8+ T cell subpopulations in the spleen. The in vivo T cell-mediated immune response of the tolerized mice was practically normal to third party CBA/Ca (H-2k) allografts. Antithymocyte autoantibodies (ATA) were detected in the sera of 76% of the tolerized mice at 1 month of age (i.e., even before the mass appearance of LPD). ATA as well as antinuclear Ab were present in 65% of the adult tolerized mice, independently of the presence of LPD. Taken together, in A mice neonatally injected with (B10 x A)F1 SC, a partial, specific allograft tolerance and a chronic host-vs.-graft disease-like syndrome developed. The latter is manifested in hyporeactivity to T cell mitogens, development of autoantibodies and, subsequently, in progressive LPD and lymphoid malignancies.

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“…In contrast to CD4 + T cells, the exogenous antigen‐specific CD8 + T cells produce IL‐10 or IL‐4 in addition to Th1‐type cytokines [5]. We have previously described the finding that bovine α s1 ‐casein, a major milk allergen, can induce specific CD8 + T cells that produce IL‐10 in addition to Th1‐type cytokines [7–11]. Our studies of artificial stimulation of the responding CD8 + T cells, such as with anti‐CD3 antibody, or dibutyryl cAMP (Bt 2 cAMP) plus a calcium ionophore, have provided evidence suggesting that separate cellular signals are required for IL‐10 or Th1‐type cytokine production [12].…”

Section: Introductionmentioning

confidence: 99%

Selective induction of CD8⁺ T cell functions by single substituted analogs of an antigenic peptide: distinct signals for IL-10 production

et al. 1998

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The CD8 + T cell clone 5F1 produces interleukin 10 (IL-10) and interferon Q Q (IFN-Q Q) in response to stimulation with a peptide corresponding to region 142^149 of bovine K K sI -casein (p142^149). Ninety analog peptides derived from p142^149 with single amino acid substitutions of putative T cell receptor contact residues were prepared to examine whether production of IL-10 and IFN-Q Q by 5F1 can be altered by stimulation with these peptides. We found that some peptides triggered only IL-10 production whereas others induced production of IFN-Q Q alone or both of these cytokines. Peptides inducing IFN-Q Q production triggered both cytotoxicity and a proliferative response, whereas peptides inducing production of IL-10 but not IFN-Q Q triggered neither of these responses. Our results clearly demonstrate that the signaling pathway required for IL-10 production in CD8 + T cells differs from that required for IFN-Q Q production. The distinct cellular signals for IL-10 production appear to be independent of those for cytotoxicity and the proliferative response of CD8 + T cells.z 1998 Federation of European Biochemical Societies.

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CD8+ Suppressor T Cell Clone 13G2 Secretes a Suppressive Lymphokine, Immune Suppressive Factor-T (ISF-T)

Cited by 3 publications

References 7 publications

Boosting Interleukin-10 Production: Therapeutic Effects and Mechanisms

Boosting Interleukin-10 Production: Therapeutic Effects and Mechanisms

Autoimmunity, hyporeactivity to T cell mitogens and lymphoproliferative disorders following neonatal induction of transplantation tolerance in mice

Selective induction of CD8⁺ T cell functions by single substituted analogs of an antigenic peptide: distinct signals for IL-10 production

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CD8+ Suppressor T Cell Clone 13G2 Secretes a Suppressive Lymphokine, Immune Suppressive Factor-T (ISF-T)

Cited by 3 publications

References 7 publications

Boosting Interleukin-10 Production: Therapeutic Effects and Mechanisms

Boosting Interleukin-10 Production: Therapeutic Effects and Mechanisms

Autoimmunity, hyporeactivity to T cell mitogens and lymphoproliferative disorders following neonatal induction of transplantation tolerance in mice

Selective induction of CD8+ T cell functions by single substituted analogs of an antigenic peptide: distinct signals for IL-10 production

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Selective induction of CD8⁺ T cell functions by single substituted analogs of an antigenic peptide: distinct signals for IL-10 production