scholarly journals Role of IL-33 and Its Receptor in T Cell-Mediated Autoimmune Diseases

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Qing Zhao ◽  
Guangjie Chen
Keyword(s):  
T Cell ◽  
Autoimmune Diseases ◽  
Host Defense ◽  
Interleukin 1 ◽  
Target Cells ◽  
Specific Receptor ◽  
Interleukin 33 ◽  
New Findings ◽  
Organ Specific

Interleukin-33 (IL-33) is a new cytokine of interleukin-1 family, whose specific receptor is ST2. IL-33 exerts its functions via its target cells and plays different roles in diseases. ST2 deletion and exclusion of IL-33/ST2 axis are accompanied by enhanced susceptibility to dominantly T cell-mediated organ-specific autoimmune diseases. It has been reported that IL-33/ST2 pathway plays a key role in host defense and immune regulation in inflammatory and infectious diseases. This review focuses on new findings in the roles of IL-33 and ST2 in several kinds of T cell-mediated autoimmune diseases.

The role of IL-12 in the induction of organ-specific autoimmune diseases

1995 ◽  
Vol 16 (8) ◽  
pp. 383-386 ◽  
Author(s):  
Sylvie Trembleau ◽  
Luciano Adorini ◽  
Tieno Germann ◽  
Maurice K. Gately
Keyword(s):  
Autoimmune Diseases ◽  
Organ Specific

scholarly journals The Role of Peptides in T Cell Alloreactivity Is Determined by Self–Major Histocompatibility Complex Molecules

2000 ◽  
Vol 191 (5) ◽  
pp. 805-812 ◽  
Author(s):  
Reinhard Obst ◽  
Nikolai Netuschil ◽  
Karsten Klopfer ◽  
Stefan Stevanović ◽  
Hans-Georg Rammensee
Keyword(s):  
T Cells ◽  
Major Histocompatibility Complex ◽  
T Cell ◽  
Target Cells ◽  
Major Histocompatibility ◽  
Complex Molecules ◽  
Mhc Molecules ◽  
Histocompatibility Complex ◽  
Alloreactive T Cells

By analyzing T cell responses against foreign major histocompatibility complex (MHC) molecules loaded with peptide libraries and defined self- and viral peptides, we demonstrate a profound influence of self-MHC molecules on the repertoire of alloreactive T cells: the closer the foreign MHC molecule is related to the T cell's MHC, the higher is the proportion of peptide-specific, alloreactive (“allorestricted”) T cells versus T cells recognizing the foreign MHC molecule without regard to the peptide in the groove. Thus, the peptide repertoire of alloreactive T cells must be influenced by self-MHC molecules during positive or negative thymic selection or peripheral survival, much like the repertoire of the self-restricted T cells. In consequence, allorestricted, peptide-specific T cells (that are of interest for clinical applications) are easier to obtain if T cells and target cells express related MHC molecules.

scholarly journals The Role of Perforin

2021 ◽  
Vol 5 (1) ◽  
pp. 75-82
Author(s):  
Davorka Švegar
Keyword(s):  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Theoretical Research ◽  
Target Cells ◽  
Colon Cancer Cell Lines ◽  
Literature Reviews ◽  
Ebsco Host ◽  
Ht 29

Some literature reviews have been carried out about the role of perforin in medicine. The first step involved a systematic search to identify relevant studies published between 2001 and 2019 in the following electronic databases - EBSCO host, Scopus, Science Direct, Web of Science, and Elsevier. By analyzing the available literature, it can be concluded that perforin plays an important role in cytoxical activity of natural killer cells (NK) and CD8+ T cell. NK and CD8+use the same mechanism for destroying target cells. This article cites the disease hemophagocytic lymphohistiocytosis (HLH) which is characterized by heavy abnormalities in the immune system. The point is that this disease is caused by perforin gene mutation. The key is the application of properly sensitized dendritic cells (DCs) because they are effective in immunotherapy against cancer. It may be effective in γ-irradiated colon cancer cell lines HT-29. Growth hormone inhibiting hormone (GIH) induces maturation and activation of DCs. In that way, GIH-Dcs shows increased cytotoxic activity and higher perforin and granzyme expression. So, this means that theoretical research has shown that efficient activity against cancer is induced when DCs are sensitized with γ-irradiated cancer cells. In that way, through a direct increase of cytotoxicity and indirect T cell activation,there can beanti-tumor activity. It is suggested to continue scientific research about the role of perforin in the future.

scholarly journals Thymus and autoimmunity: capacity of the normal thymus to produce pathogenic self-reactive T cells and conditions required for their induction of autoimmune disease.

1990 ◽  
Vol 172 (2) ◽  
pp. 537-545 ◽  
Author(s):  
S Sakaguchi ◽  
N Sakaguchi
Keyword(s):  
Bone Marrow ◽  
T Cells ◽  
Bone Marrow Transplantation ◽  
T Cell ◽  
Autoimmune Disease ◽  
Autoimmune Diseases ◽  
Rheumatoid Factors ◽  
Systemic Autoimmune Diseases ◽  
Organ Specific ◽  
Gastric Parietal Cells

BALB/c athymic nu/nu mice spontaneously developed organ-specific (gastritis, thyroiditis, oophoritis, or orchitis) and systemic (arteritis, glomerulonephritis, and polyarthritis) autoimmune diseases when transplanted with neonatal BALB/c thymuses. Transplantation of thymuses from adult BALB/c mice was far less effective in inducing histologically evident organ-specific autoimmune disease in nu/nu mice. Autoimmune disease developed, however, when adult thymuses were irradiated at a T cell-depleting dose before transplantation. Engrafting newborn thymuses into BALB/c mice T cell depleted by thymectomy, irradiation, and bone marrow transplantation produced similar organ-specific autoimmune disease as well, but thymus engrafting into T cell-nondepleted BALB/c mice (i.e., mice thymectomized as adults, but not irradiated) did not, despite the fact that transplanted thymuses grew well in both groups of mice. The mice with organ-specific autoimmune disease produced autoantibodies specific for the respective organ components, such as gastric parietal cells, thyroglobulins, oocytes, or sperm. The thymus-transplanted nu/nu mice also had hypergammaglobulinemia and developed anti-DNA autoantibodies, rheumatoid factors, and immune complexes in the circulation. These results indicate that: (a) the thymus of a murine strain that does not develop spontaneous autoimmune disease can produce pathogenic self-reactive T cells that mediate organ-specific and/or systemic autoimmune diseases; and (b) such self-reactive T cells, especially those mediating organ-specific autoimmune disease, spontaneously expand and cause autoimmune disease when released to the T cell-deficient or -eliminated periphery.

Cytotoxicity against lymphoblastoid cells mediated by a T-cell clone from an aplastic anaemia patient: role of CD59 on target cells

1999 ◽  
Vol 107 (4) ◽  
pp. 791-796 ◽  
Author(s):  
Akiyoshi Takami ◽  
Weihua Zeng ◽  
Hongbo Wang ◽  
Tamotsu Matsuda ◽  
Shinji Nakao
Keyword(s):  
T Cell ◽  
Aplastic Anaemia ◽  
Cell Clone ◽  
Target Cells ◽  
Lymphoblastoid Cells ◽  
Patient Role ◽  
T Cell Clone

scholarly journals Role of IL-38 and Its Related Cytokines in Inflammation

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Xianli Yuan ◽  
Xiao Peng ◽  
Yan Li ◽  
Mingcai Li
Keyword(s):  
T Cell ◽  
Immune Responses ◽  
Receptor Antagonist ◽  
Inflammatory Responses ◽  
Structural Features ◽  
Specific Receptor ◽  
Anti Inflammatory ◽  
Near Future

Interleukin- (IL-) 38 is a recently discovered cytokine and is the tenth member of the IL-1 cytokine family. IL-38 shares structural features with IL-1 receptor antagonist (IL-1Ra) and IL-36Ra. IL-36R is the specific receptor of IL-38, a partial receptor antagonist of IL-36. IL-38 inhibits the production of T-cell cytokines IL-17 and IL-22. IL-38 also inhibits the production of IL-8 induced by IL-36γ, thus inhibiting inflammatory responses. IL-38-related cytokines, including IL-1Ra and IL-36Ra, are involved in the regulation of inflammation and immune responses. The study of IL-38 and IL-38-related cytokines might provide new insights for developing anti-inflammatory treatments in the near future.

Role of interferon-γ in Vα14+ natural killer T cell-mediated host defense against Streptococcus pneumoniae infection in murine lungs

2007 ◽  
Vol 9 (3) ◽  
pp. 364-374 ◽  
Author(s):  
Masashi Nakamatsu ◽  
Natsuo Yamamoto ◽  
Masumitsu Hatta ◽  
Chikara Nakasone ◽  
Takeshi Kinjo ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
T Cell ◽  
Natural Killer ◽  
Host Defense ◽  
Interferon Γ ◽  
Natural Killer T Cell ◽  
Killer T Cell ◽  
Natural Killer T

scholarly journals Impaired response to Listeria in H2-M3–deficient mice reveals a nonredundant role of MHC class Ib–specific T cells in host defense

2006 ◽  
Vol 203 (2) ◽  
pp. 449-459 ◽  
Author(s):  
Honglin Xu ◽  
Taehoon Chun ◽  
Hak-Jong Choi ◽  
Bin Wang ◽  
Chyung-Ru Wang
Keyword(s):  
T Cells ◽  
T Cell ◽  
Host Defense ◽  
Cd8 T Cells ◽  
Mhc Class Ib ◽  
Cell Responses ◽  
Mhc Class Ia ◽  
Deficient Mice ◽  
Class Ib

The major histocompatibility complex (MHC) class Ib molecule H2-M3 primes the rapid expansion of CD8+ T cells by presenting N-formylated bacterial peptides. However, the significance of H2-M3–restricted T cells in host defense against bacteria is unclear. We generated H2-M3–deficient mice to investigate the role of H2-M3 in immunity against Listeria monocytogenes (LM), a model intracellular bacterial pathogen. H2-M3–deficient mice are impaired in early bacterial clearance during primary infection, with diminished LM-specific CD8+ T cell responses and compromised innate immune functions. Although H2-M3–restricted CD8+ T cells constitute a significant proportion of the anti-listerial CD8+ T cell repertoire, the kinetics and magnitude of MHC class Ia–restricted T cell responses are not altered in H2-M3–deficient mice. The fact that MHC class Ia–restricted responses cannot compensate for the H2-M3–mediated immunity suggests a nonredundant role of H2-M3 in the protective immunity against LM. Thus, the early H2-M3–restricted response temporally bridges the gap between innate and adaptive immune responses, subsequently affecting the function of both branches of the immune system.

Sign in / Sign up

Export Citation Format

Share Document