[PDF] Transforming Growth Factor β (TGF-β)-dependent Inhibition of T Helper Cell 2 (Th2)-induced Autoimmunity by Self–Major Histocompatibility Complex (MHC) Class II–specific, Regulatory CD4+ T Cell Lines | Semantic Scholar (2024)

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Treatment with CD3ε-specific antibodies induces transferable T-cell-mediated tolerance involving CD4+CD25+ cells, which places them as the first clinically applicable pharmacological stimulant of TGF-β-producing regulatoryCD4+ T cells.

Another evidence for the existence of regulatory T cells in the T lymphocyte repertoire is offered, suggesting that they can also regulate immune responses to foreign antigens.

It is shown that transforming growth factor (TGF)- (cid:98) and interleukin (IL)-4 both play essential roles in the mechanism of this protection since administration of monoclonal antibodies that block the biological activity of either of these cytokines abrogates the protective effect of the donor cells in the recipient rats.

Evidence is provided to support the phenotypic and functional diversity of regulatory T cells mediating transferable ‘active’ or ‘dominant’ peripheral tolerance in the non‐obese diabetic mouse model (NOD) and the working hypothesis they evoke is discussed.

It is demonstrated that specialized subsets of regulatory T cells are pivotal in the control of autoimmune diabetes as well shown by the compelling evidence accumulated using the non-obese diabetic (NOD) mouse model.

Evidence is brought about showing that Tr1 cells play a pivotal role in the regulation of T cell tolerance during determinant spread and that soluble peptide therapy with the determinant to which the autoimmune response spreads amplifies a de novo regulatory mechanism aimed to reduce the pathological consequences of determinant spreading.

It is proposed that dysregulated expansion of potentially pathogenic T cells in a lymphopenic environment can be prevented by members of the naive T cell repertoire, irrespective of their specificity, as a side effect of their response to homeostatic and antigenic stimulation.

Dasatinib treatment was associated with a significant reduction in the levels of biomarkers and with an increased incidence of LGLs compared with imatinib or nilotinib treatment, both of which are related to immunological conditions.

Genome-wide searches in the rat have shown that overlapping chromosomal regions control the immunological disorders induced by gold salt treatment, the development of experimental autoimmune encephalomyelitis and the CD45RC(high)/CD 45RC(low)CD4(+)T cells balance, which should help to improve efficacy and safety of vaccines.

Results show that DNA vaccination could be used as a method to specifically manipulate a T cell response and thus prolong allograft survival in a transplantation model.

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A subpopulation of peripheral CD4+ cells and TGF-beta are identified as critical components of the natural immune regulatory mechanism, which prevents the development of pathogenic Th1 responses in the gut, and it is suggested that this immunoregulatory population is distinct from Th2 cells.

It is concluded that HgCl2 induces CD4+ autoreactive T cells that proliferate in the presence of class II+ cells in susceptible BN as well as in resistant LEW rats.

The ability of autoreactive Th2 as well as Th0 cell lines to induce antibody‐mediated autoimmunity is demonstrated for the first time and it is suggested that Th2 cells could initiate cell‐mediated reactions either directly or indirectly.

This work addressed the role of the Thl‐like subset in this disease and found that increase in major histocompatibility complex class II molecule expression on B cells concomitant with enhancement of serum IgE concentration supports the involvement of the T helper 2 (Th2)‐ like subset in the induction of the disease.

It is demonstrated that HgCl2 has very early direct effects on cytokine production and that these effects differ depending on the strain, and the early effect on IL-4 production observed on BN rat spleen cells and T cells may explain that the autoreactive anti-class II T cells that are found in HGCl2-injected BN rats have a Th2 phenotype.

It is concluded that autoreactive BNY-2 T cells, established from the pancreatic islets of acutely diabetic BB rats, can prevent the development of autoimmune diabetes in the diabetes-prone BB rat by an immunosuppressive effect.

It is concluded that autoreactive T cells, and presumably anti-Ia T cells are involved in the pathogenesis of mercury-induced autoimmunity.

It is concluded that the protective effect of TGF-beta is exerted at the level of the target organ, CNS and/or its vascular endothelium, rather than through a direct effect on lymphoid cells, and that there is a small window of 4 days in which T GF-beta exerts its protective effect.

Mucosally derived TH2-like clones induced by oral antigen can actively regulate immune responses in vivo and may represent a different subset of T cells.

Observations demonstrate that manipulation of lymphocyte accessory counterreceptor interactions may affect the course of Th2- associated autoimmune disease and suggest that signals resulting from CD2 engagement play an essential role in the regulation of the Th1-Th2 effector equilibrium.

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