Aqueous antigens induce in vivo tolerance selectively in IL-2- and IFN-gamma-producing (Th1) cells.

Burstein, Harold J.; Shea, Colleen M.; Abbas, Abul K.

doi:10.4049/jimmunol.148.12.3687

Cited by 141 publications

(3 citation statements)

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“…Helper T cells are the important immune cells mediating inflammatory response [14], which can be divided into Th1 and Th2 cells that exert different immune effects [15,16]. Th1 cells are mainly dependent on IL-2 and IFN-γ [17], induce the macrophage-dependent immune response, enhance the toxic effect of natural killer (NK) cells, and mediate hypersensitivity reaction to cause tissue injury [18]. Th2 cells mainly secrete IL-4 and IL-10, which can promote the IgE-mediated hypersensitivity reaction and humoral immune response [19].…”

Section: Discussionmentioning

confidence: 99%

Th1 promotes M1 polarization of intestinal macrophages to regulate colitis-related mucosal barrier damage

Ruan

Sheng

et al. 2023

Aging

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This work aimed to investigate the role of helper T cell 1 (Th1) in chronic colitis and its immunoregulatory mechanism. The proportions of Th1 and Th2, and the levels of related cytokines in tissues from patients with inflammatory bowel disease (IBD; ulcerative colitis+Crohn's disease, UC+CD) were detected. DSS was used to induce the mouse model of IBD; thereafter, Th1 cells were induced in vitro and amplified before they were injected intraperitoneally. Later, the changes in life state and body weight of mice were observed, the proportion of M1 macrophages in mucosal tissues and mucosal barrier damage were detected. After treatment with macrophage scavenging agent (Clodronate Liposomes, CLL), the influence of Th1 on IBD mice was observed. Then, the intestinal macrophages were co-cultured with Th1 in vitro to observe the influence of Th1 on the polarization of intestinal macrophages. Besides, cells were treated with the STAT3 inhibitor to further detect the macrophage polarization level. Intestinal macrophages were later co-cultured with intestinal epithelial cells to observe the degree of epithelial cell injury. The Th1 proportions in intestinal tissues of UC and CD patients were higher than those in healthy subjects, but the difference in Th2 proportion was not significant. In the IBD mouse model, Th1 induced the M1 polarization of macrophages, aggravated the intestinal inflammatory response, and resulted in the increased mucosal barrier permeability. Pretreatment with CLL antagonized the effect of Th1 cells, reduced the intestinal tissue inflammatory response and mucosal barrier permeability.

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Section: Discussionmentioning

confidence: 99%

Th1 promotes M1 polarization of intestinal macrophages to regulate colitis-related mucosal barrier damage

Ruan

Sheng

et al. 2023

Aging

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“…Previous studies have discovered that peripheral inflammation is related to the peripheral T lymphocytes-secreted cytokines [ 12 , 13 ]. Th1 and Th2 are the two important subsets of Th cells, Th1 cells mainly secrete the pro-inflammatory cytokines to participate in macrophage activation for mediating cellular immunity [ 14 , 15 ], such as interleukin-6 (IL-6) [ 16 ], Interferon-γ (IFN-γ) [ 17 ]. By contrast, Th2 cells mainly secrete inhibitory cytokines like IL-4 and IL-10 [ 18 , 19 ] to mediate humoral immunity.…”

Section: Discussionmentioning

confidence: 99%

PCSK6 mediates Th1 differentiation and promotes chronic colitis progression and mucosal barrier injury via STAT1

Mei

Zhou

Song

et al. 2023

Aging

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This study was aimed at investigating the expression and role of proprotein convertase subtilisin/kexin type (PCSK6) in inflammatory bowel disease (IBD). DSS induced mouse colitis and mucosal barrier injury, down-regulation of TJ proteins, improvement of permeability, and increases of the proportions of Th1 and M1 macrophages. After PCSK6 knockdown, the colitis in KO mice was improved relative to WT mice, the TJ protein levels increased, and the proportions of Th1 and M1 macrophages decreased. STAT1 inhibitor treatment also inhibited chronic colitis in mice. As revealed by in-vitro experiments, PCSK6 overexpression promoted the transformation of Th0 into Th1, while PCSK6 silencing suppressed the transfection. COPI assay results revealed the presence of targeted binding relation between PCSK6 and STAT1. PCSK6 binds to STAT1 to promote STAT1 phosphorylation and regulate Th1 cell differentiation, thus promoting the M1 polarization of macrophages and aggravating colitis progression. PCSK6 is promising as the new target for the treatment of colitis.

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“…TGF-β) (26), and (iii) dysregulation between T h 1 and T h 2 cells (10). Considering the third possibility, it has been reported that T h 1 cells are more likely to be anergized than T h 2 cells (27). Therefore, oral tolerance has been shown to reflect preferential activation of T h 2 cells with subsequent downregulation of T h 1 responses (28).…”

Section: Discussionmentioning

confidence: 99%

Human milk proteins including secretory IgA fail to elicit tolerance after feeding

Yuki

Fujihashi²,

Yamamoto³

et al. 1998

International Immunology

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Oral administration of large doses of protein antigen generally induces a state of systemic unresponsiveness currently termed mucosally induced tolerance. In this study, we used human milk protein (HMP) without casein as a multi-protein antigen for the study of mucosally induced tolerance. The HMP utilized in this study mainly contained secretory (S) IgA, lactoferrin (Lf) and alpha-lactalbumin (Lact). When mice were given 1 or 25 mg of HMP orally 3 times or 25 mg orally four consecutive weeks prior to systemic immunization, antigen-specific serum IgG responses to HMP were induced by subsequent parenteral immunization with 100 microg of HMP. Analysis of IgG subclasses revealed that IgG1 followed by IgG2b accounted for the IgG responses noted. When both HMP and ovalbumin (OVA) were fed to mice, tolerance developed to OVA but not to HMP. To further investigate the nature of immune responses seen following oral gavage of HMP, we examined responses to individual protein of HMP. Brisk serum IgG1 and IgG2b responses to both S-IgA and Lf were induced by oral followed by systemic immunization with HMP. Analysis of splenic CD4+ T cells from mice given oral HMP revealed production of Th2- but not Th1-type cytokines. These results show that oral administration of HMP preferentially induces exclusive Th2-type immune responses, which may prevent the development of HMP (S-IgA and Lf)-specific mucosally induced tolerance.

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Aqueous antigens induce in vivo tolerance selectively in IL-2- and IFN-gamma-producing (Th1) cells.

Cited by 141 publications

References 0 publications

Th1 promotes M1 polarization of intestinal macrophages to regulate colitis-related mucosal barrier damage

Th1 promotes M1 polarization of intestinal macrophages to regulate colitis-related mucosal barrier damage

PCSK6 mediates Th1 differentiation and promotes chronic colitis progression and mucosal barrier injury via STAT1

Human milk proteins including secretory IgA fail to elicit tolerance after feeding

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