Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

House dust mites provide well-characterized proteins to study human responses to inhaled antigens. Even in the absence of allergy they induce a high frequency of T cell precursors. The healthy response manifests by T cell proliferation and Th1 cytokines with little antibody. Responses of allergic people include Th1 and Th2 cytokines and IgE, IgG1, and IgG4 antibodies. Regulatory cells limit effector responses in healthy people. About half the IgE and IgG antibodies bind the group 1 and 2 allergens and 30% bind the group 4, 5, and 7 allergens. Although HLA independent, the recognition of the group 1 allergen shows an immunodominant region and a T cell receptor bias. The major allergens are not produced in higher amounts than many of the poorly non-allergenic proteins. The non-allergenic mite ferritin antigen shows high T cell proliferative responses with mixed cytokine production.
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PMID:T and B cell responses to HDM allergens and antigens. 1787 3

Mycoplasma arthritidis causes arthritis in specific mouse strains. M. arthritidis mitogen (MAM), a superantigen produced by M. arthritidis, activates T cells by forming a complex between the major histocompatability complex II on antigen presenting cells and the T cell receptor on CD4+ T lymphocytes. The MAM superantigen is also known to interact with Toll-like receptors (TLR) 2 and 4. Hepcidin, an iron regulator protein, is upregulated by TLR4, IL-6, and IL-1. In this study, we evaluated serum hepcidin, transferrin saturation, ferritin, IL-6, IL-1, and hemoglobin levels in M. arthritidis injected C3H/HeJ (TLR2+/+, TLR4-/-) mice and C3H/HeSnJ (TLR2+/+, TLR4+/+) mice over a 21 day period. C3H/HeJ mice have a defective TLR4 and an inability to produce IL-6. We also measured arthritis severity in these mice and the amount of hepcidin transcripts produced by the liver and spleen. C3H/HeJ mice developed a more severe arthritis than that of C3H/HeSnJ mice. Both mice had an increase in serum hepcidin within three days after infection. Hepcidin levels were greater in C3H/HeJ mice despite a nonfunctioning TLR4 and low serum levels of IL-6. Splenic hepcidin production in C3H/HeJ mice was delayed compared to C3H/HeSnJ mice. Unlike C3H/HeSnJ mice, C3H/HeJ mice did not develop a significant rise in serum IL-6 levels but did develop a significant increase in IL-1beta during the first ten days after injection. Both mice had an increase in serum ferritin but a decrease in serum transferrin saturation. In conclusion, serum hepcidin regulation in C3H/HeJ mice does not appear to be solely dependent upon TLR4 or IL-6.
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PMID:Hepcidin is elevated in mice injected with Mycoplasma arthritidis. 1993 Jul 11

Epstein-Barr virus (EBV) is the pathogen that most commonly triggers infection-associated hemophagocytic lymphohistiocytosis (HLH) and ectopically infects CD8(+) T cells in EBV-associated HLH (EBV-HLH). We recently described an EBV-HLH patient who had a clonally expanded population of EBV-infected CD8(+) T cells with CD5 down-regulation. To determine whether this finding could serve as a useful marker for EBV-HLH, we investigated 5 additional patients. We found a significant increase in the subpopulation of CD8(+) T cells with CD5 down-regulation and bright human leukocyte antigen (HLA)-DR expression in all patients with EBV-HLH but not in patients with infectious mononucleosis or in control subjects. Such T cells were frequently found to be larger cells that stained positive for a specific T cell receptor VB. We also demonstrated that those cells were the major cellular target of EBV, and their numbers progressively declined in parallel with the serum ferritin levels. All together, our findings reveal the immunophenotypic characteristics of EBV-infected CD8(+) T cells and may provide a valuable tool for the diagnosis of EBV-HLH.
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PMID:Clinical significance of cloned expansion and CD5 down-regulation in Epstein-Barr Virus (EBV)-infected CD8+ T lymphocytes in EBV-associated hemophagocytic lymphohistiocytosis. 2044 35

The study was undertaken to decipher the microRNA (miRNA) related markers associated with corpus luteum (CL) tropism in buffalo. The data obtained from deep sequencing of CL tissue from different physiological stages was mined in silico for the identification of miRNA-related markers (SSR & SNP). From the present study, 5 annotated and 176 unannotated miRNA were deduced while comparing with Bos taurus genome. In addition, 4 SSRs and 9 SNPs were deduced from the miRNA sequences. These SSRs were on the genes viz. Eukaryotic translation initiation factor 1-like, myocyte enhancer factor 2A, beta casein, T cell receptor gamma cluster 1. The SNP positions on genes viz. PYGO1 (Pygopus family PHD finger 1), LOC100337244 (Multidrug resistance-associated protein 4), FTH1 (Ferritin heavy chain 1), LOC788634 (BOLA class I histocompatibility antigen), PLXND1 (Plexin D1) and UBC (Ubiquitin C) show that these genes play critical role in CL tropism during estrous cycle in buffalo.
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PMID:MicroRNA-related markers associated with corpus luteum tropism in buffalo (Bubalus bubalis). 3073 93