介绍了Kirk—Othmer Encyclopedia of Chemical Technology（化工技术百科全书）（第五版）电子图书网络版数据库，并对该数据库使用方法和检索途径作出了说明，且结合实例简单地介绍了该数据库的检索方法。

Kirk-Othmer Encyclopedia of Chemical Technology数据库介绍及实例

Complete list of abbreviations of tumor antigens 707-AP 707 alanine proline-AFP alpha (α)-fetoprotein-ART-4 adenocarcinoma antigen recognized by T cells 4 BAGE B antigen-β-catenin/m β-catenin/mutated-Bcr-abl breakpoint cluster region-Abelson - CAMEL CTL-recognized antigen on melanoma CAP-1 carcinoembryonic antigen peptide-1-CASP-8 caspase-8 CDC27m cell-division-cycle 27 mutated-CDK4/m cycline-dependent kinase 4 mutated-CEA carcino-embryonic antigen-CT cancer/testis (antigen)-Cyp-B cyclophilin B DAM differentiation antigen melanoma (the epitopes of DAM-6 and DAM-10 are equivalent, but the gene sequences are different; DAM-6 is also called MAGE-B2. and DAM-10 is also called MAGE-B1) ELF2M elongation factor 2 mutated ETV6-AML1 Ets variant gene 6/acute myeloid leukemia 1 gene ETS G250 glycoprotein 250 - GAGE G antigen GnT-V N-acetylglucosaminyltransferase V -Gp100 glycoprotein 100 kDa-HAGE helicose antigen-HER-2/neu human epidermal receptor-2/ neurological - HLA-A * 0201-R1701 arginine (R) to isoleucine (I) exchange at residue 170 of the α-helix of the α2-domain in the HLA-A2 gene HPV-E7 human papilloma virus E7 HSP70-2M heat shock protein 70-2 mutated HST-2 human signet ring tumor-2 hTERT or hTRT human telomerase reverse transcriptase-iCE intestinal carboxyl esterase KIAA0205 name of the gene as it appears in databases-LAGE L antigen LDLR/FUT low-density lipid receptor/GDP-L-fucose: β-D-galactosidase 2-α-L-fucosyltransferase MAGE melanoma antigen MART-1/Melan-A melanoma antigen recognized by T cells-1/melanoma antigen A MC1R melanocortin 1 receptor Myosin/m myosin mutated-MUC1 mucin 1-MUM-1, -2, -3 melanoma ubiquitous mutated 1, 2, 3 NA88-A NA cDNA clone of patient M88-NY-ESO-1 New York-esophagus 1 - P15 protein 15 p190 minor bcr-abl protein of 190 kDa ber-abl Pml/RARα promyelocytic leukaemia/retinoic acid receptor α-PRAME preferentially expressed antigen of melanoma PSA prostate-specific antigen-PSM prostate-specific membrane antigen-RAGE renal antigen RU1 or RU2 renal ubiquitous 1 or 2 SAGE sarcoma antigen SART-1 or SART-3 squamous antigen rejecting tumor 1 or 3-TEL/ AML1 translocation Ets-family leukemia/acute myeloid leukemia 1 TPI/m triosephosphate isomerase mutated TRP-1 tyrosinase related protein 1, or gp75 TRP-2 tyrosinase related protein 2 TRP-2/ INT2 TRP-2/intron 2 WT1 Wilms' tumor gene Abbreviations used ALL acute lymphoblastic leukemia AML acute myeloid leukemia-APL acute promyelocytic leukemia-CML chronic myelogenous leuke mia-CTL cytotoxic T lymphocytes-Ets E-26 transforming specific (family of transcription factors) H/N head and neck-MHC major histocompatibility complex-NSCLC non-small cell lung carcinoma-ORF open reading frame RCC renal cell carcinoma-SCC squamous cell carcinoma-TSTA tumor-specific transplantation antigens.

/pdf/a-listing-of-human-tumor-antigens-recognized-by-t-cells-1tq0i7ajhz.pdf

A listing of human tumor antigens recognized by T cells.

Leishmaniasis is caused by an intracellular parasite transmitted to humans by the bite of a sand fly. It is endemic in Asia, Africa, the Americas, and the Mediterranean region. Worldwide, 1.5 to 2 million new cases occur each year, 350 million are at risk of acquiring the disease, and leishmaniasis causes 70,000 deaths per year. Clinical features depend on the species of Leishmania involved and the immune response of the host. Manifestations range from the localized cutaneous to the visceral form with potentially fatal outcomes. Many drugs are used in its treatment, but the only effective treatment is achieved with current pentavalent antimonials.

/pdf/leishmaniasis-a-review-tvy2f07zgf.pdf

Leishmaniasis: a review.

Coumarins are a very large family of compounds containing the unique 2H-chromen-2-one motif, as it is known according to IUPAC nomenclature. Coumarin derivatives are widely found in nature, especially in plants and are constituents of several essential oils. Up to now, thousands of coumarin derivatives have been isolated from nature or produced by chemists. More recently, the coumarin platform has been widely adopted in the design of small-molecule fluorescent chemosensors because of its excellent biocompatibility, strong and stable fluorescence emission, and good structural flexibility. This scaffold has found wide applications in the development of fluorescent chemosensors in the fields of molecular recognition, molecular imaging, bioorganic chemistry, analytical chemistry, materials chemistry, as well as in the biology and medical science communities. This review focuses on the important progress of coumarin-based small-molecule fluorescent chemosensors during the period of 2012-2018. This comprehensive and critical review may facilitate the development of more powerful fluorescent chemosensors for broad and exciting applications in the future.

Coumarin-Based Small-Molecule Fluorescent Chemosensors.

The role of redox molecules, such as NO and ROS, as key mediators of immunity has recently garnered renewed interest and appreciation. To regulate immune responses, these species trigger the eradication of pathogens on the one hand and modulate immunosuppression during tissue-restoration and wound-healing processes on the other. In the acidic environment of the phagosome, a variety of RNS and ROS is produced, thereby providing a cauldron of redox chemistry, which is the first line in fighting infection. Interestingly, fluctuations in the levels of these same reactive intermediates orchestrate other phases of the immune response. NO activates specific signal transduction pathways in tumor cells, endothelial cells, and monocytes in a concentration-dependent manner. As ROS can react directly with NO-forming RNS, NO bioavailability and therefore, NO response(s) are changed. The NO/ROS balance is also important during Th1 to Th2 transition. In this review, we discuss the chemistry of NO and ROS in the context of antipathogen activity and immune regulation and also discuss similarities and differences between murine and human production of these intermediates.

https://jlb.onlinelibrary.wiley.com/doi/pdf/10.1189/jlb.1010550

Nitric oxide and redox mechanisms in the immune response

Thrombospondins (TSPs) have been implicated as antitumor and antimetastasis factors in breast cancer. Although this effect has been attributed to the antiangiogenic activity of TSPs, recent observations suggest other mechanisms may be at work. The TSP receptor CD47 (integrin-associated protein) has recently been reported to mediate a novel form of apoptosis. Here, we have studied the response of breast cancer cells to CD47 ligands TSP-1, the CD47 agonist peptide 4N1K derived from TSP-1, and the anti-CD47 monoclonal antibody 1F7. All of these ligands killed four different breast cancer cell lines. This CD47-mediated cell death did not require active caspases or Bcl-2 degradation and did not cause DNA laddering or cytochrome c release. Pertussis toxin (PTX) prevented CD47-mediated death, indicating the involvement of Giα. 4N1K dramatically reduced intracellular cAMP levels, an effect reversed with PTX. Forskolin, 8-bromo cAMP, and isobutylmethylxanthine (IBMX) all prevented CD47-mediated apoptosis, indicating the involvement of cAMP. H89 and protein kinase A (PKA) inhibitor peptide prevented rescue of breast cancer cells by PTX, 8-Br-cAMP, and forskolin, suggesting that the effects of cAMP are mediated via PKA-dependent phosphorylation events. Epidermal growth factor also inhibited CD47-induced apoptosis via a PKC-dependent but ERK-independent pathway. Thus, CD47-mediated killing of breast cancer cells occurs by a novel pathway involving regulation of cAMP levels by heterotrimeric Gi with subsequent effects mediated by PKA.

https://cancerres.aacrjournals.org/content/canres/64/3/1026.full.pdf

CD47 Mediates Killing of Breast Tumor Cells via Gi-Dependent Inhibition of Protein Kinase A

CD47 has been implicated in both positive and negative regulation of T cells as well as in T cell death. To clarify the role of CD47 in T cell function, we have studied the mechanism of T cell death in response to CD47 ligands, including mAb 1F7, thrombospondin-1, and a CD47 agonist peptide derived from it. CD47 −/− Jurkat T cells (JINB8) were resistant to killing by all three ligands, indicating the essential role of CD47. Primary human T cells were also killed by CD47 ligands, but only after activation with anti-CD3. CD47-mediated cell death occurred without active caspases, DNA fragmentation, or Bcl-2 degradation. Pretreatment of Jurkat and primary T cells with pertussis toxin (PTX) prevented CD47-mediated death, indicating the involvement of G iα . Pretreatment of T cells with 8-bromo cAMP, forskolin, or 3-isobutyl-1-methylxanthine prevented the CD47-mediated apoptosis, and 1F7 dramatically reduced intracellular cAMP levels, an effect reversed with PTX. H89 and protein kinase A (PKA) inhibitor peptide, a specific PKA inhibitor, prevented rescue of T cells by PTX, 8-bromo cAMP, and forskolin, indicating a direct role for one or more PKA substrates. Thus, CD47-mediated killing of activated T cells occurs by a novel pathway involving regulation of cAMP levels by heterotrimeric G iα with subsequent effects mediated by PKA.

The Mechanism of CD47-Dependent Killing of T Cells: Heterotrimeric Gi-Dependent Inhibition of Protein Kinase A

CD47 augments Fas/CD95-mediated apoptosis.

CD47 is a ubiquitously expressed cell surface glycoprotein that associates with integrins and regulates chemotaxis, migration, and activation of leukocytes. CD47 is also a ligand for signal regulatory protein alpha, a cell surface receptor expressed on monocytes, macrophages, granulocytes, and dendritic cell (DC) subsets that regulates cell activation, adhesion, and migration. Although the function of CD47 in macrophages and granulocytes has been studied in detail, little is known about the role of CD47 in DC biology in vivo. In this study we demonstrate that CD47(-/-) mice exhibit a selective reduction of splenic CD11c(high)CD11b(high)CD8alpha(-)CD4(+) DCs. These DCs correspond to marginal zone DCs and express signal regulatory protein alpha, possibly explaining their selective deficiency in CD47(-/-) mice. Deficiency of marginal zone DCs resulted in impairment of IgG responses to corpusculate T cell-independent Ags. Although epidermal DCs were present in normal numbers in CD47(-/-) mice, their migration to draining lymph nodes in response to contact sensitization was impaired, while their maturation was intact. In vitro, CD47(-/-) mature DCs showed normal CCR7 expression but impaired migration to CCL-19, whereas immature DC response to CCL-5 was only slightly impaired. These results demonstrate a fundamental role of CD47 in DC migration in vivo and in vitro and in the function of marginal zone DCs.

Deficit of CD47 results in a defect of marginal zone dendritic cells, blunted immune response to particulate antigen and impairment of skin dendritic cell migration.

Mammaglobin-A is highly overexpressed in breast cancer cell lines and primary breast tumors This pattern of expression is restricted to mammary epithelium and metastatic breast tumors Thus, mammaglobin-A-specific T cell immune responses may provide an important approach for the design of breast cancer-specific immunotherapy The purpose of our study was to define the T cell-mediated immune response to mammaglobin-A We determined that the frequency of mammaglobin-A-reactive CD8+ and CD4+ T cells in breast cancer patients is significantly higher than that observed in healthy female controls using limiting dilution analyses (p = 0026 and p = 002, respectively) We identified 8 mammaglobin-A-derived 9-mer peptides with the highest binding affinity for the HLA-A3 molecule (Mam-A31-8) using a computer-assisted analysis of the mammaglobin-A protein sequence Subsequently, we determined that CD8+ T cells from breast cancer patients reacted to peptides Mam-A31 (23-31, PLLENVISK), Mam-A33 (2-10, KLLMVLMLA), Mam-A34 (55-63, TTNAIDELK) and Mam-A38 (58-66, AIDELKECF) using an IFN-gamma enzyme-linked immunospot assay A CD8+ T cell line generated in vitro against HLA-A*0301-transfected TAP-deficient T2 cells loaded with these peptides showed significant cytotoxic activity against the Mam-A31 peptide This CD8+ T cell line showed a significant HLA-A3-restricted cytotoxic activity against mammaglobin-A-positive but not mammaglobin-A-negative breast cancer cells In summary, our study identified four HLA-A3-restricted mammaglobin-A-derived epitopes naturally expressed by breast cancer cells, indicating the immunotherapeutic potential of this novel antigen for the treatment and prevention of breast cancer

Partha Pratim Manna

Papers

CD47 Mediates Killing of Breast Tumor Cells via Gi-Dependent Inhibition of Protein Kinase A

The Mechanism of CD47-Dependent Killing of T Cells: Heterotrimeric Gi-Dependent Inhibition of Protein Kinase A

CD47 augments Fas/CD95-mediated apoptosis.

Deficit of CD47 results in a defect of marginal zone dendritic cells, blunted immune response to particulate antigen and impairment of skin dendritic cell migration.

Identification of HLA-A3-restricted CD8+ T cell epitopes derived from mammaglobin-A, a tumor-associated antigen of human breast cancer.