Seracare恰加斯病/南美錐蟲 Chagas
| 型 號： | 美國 |
| 報 價： |  |
美國Seracare恰加斯病/南美錐蟲 Chagas 陽性質(zhì)控品對照品 需要了解更多Seracare產(chǎn)品可以咨詢我們，本產(chǎn)品由廣州健侖生物科技有限公司提供
- 產(chǎn)品描述
美國Seracare恰加斯病/南美錐蟲 Chagas
廣州健侖生物科技有限公司
廣州健侖長期供應(yīng)各種生物原料，主要代理品牌：美國Seracare、西班牙Certest、美國Fuller等等。
主要產(chǎn)品包括各種標(biāo)準(zhǔn)品、陽性對照品、單克隆抗原抗體。
其中常見的有：弓形蟲病、西尼羅河病毒、類風(fēng)濕因子、瘧疾、麻疹、萊姆病、百日咳桿菌、大腸桿菌、鼠傷寒沙門氏菌、李斯特菌等陽性對照品。
美國Seracare恰加斯病/南美錐蟲 Chagas
我司還提供其它進口或國產(chǎn)試劑盒：登革熱、瘧疾、流感、A鏈球菌、合胞病毒、腮病毒、乙腦、寨卡、黃熱病、基孔肯雅熱、克錐蟲病、違禁品濫用、肺炎球菌、軍團菌、化妝品檢測、食品安全檢測等試劑盒以及日本生研細(xì)菌分型診斷血清、德國SiFin診斷血清、丹麥SSI診斷血清等產(chǎn)品。
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【Seracare產(chǎn)品介紹】
編號 | 英文名稱 | 中文名稱 |
JL-FA-01 | Amebiasis (AME) | 阿米巴病 |
JL-FA-02 | Allergens, Rast scores | 過敏原，放射性過敏原吸收實驗。指對特定的人群引起免疫反應(yīng)或者過敏反應(yīng)的食品中的蛋白質(zhì) |
JL-FA-03 | Allergens, Rast scores negative | 過敏原，放射性過敏原吸收實驗陰性 |
JL-FA-04 | Anti-cyclic citrullinated peptide Antibody (CCP) Arthritis | 抗環(huán)瓜氨酸肽抗體 |
JL-FA-05 | ASCA Saccharomyces Cerevi | 人抗釀酒酵母抗體（ASCA） |
JL-FA-06 | Aspergillis | 麴菌病 |
JL-FA-07 | Beta 2 Glycoprotein | β2糖蛋白 |
JL-FA-08 | Beta 2 Glycoprotein IgM | β2糖蛋白 IGM |
JL-FA-09 | Bordela Pertussis | 百日咳桿菌 |
JL-FA-10 | Bordela Pertussis IgM | 百日咳桿菌 IGM |
JL-FA-11 | C-ANCA | C-抗中性粒細(xì)胞胞漿抗體（ANCA) |
JL-FA-12 | Cardiolipin | 心肌磷脂 |
JL-FA-13 | Cardiolipin IgA | 心肌磷脂 IGA |
JL-FA-14 | Cardiolipin IgG | 心肌磷脂 IGG |
JL-FA-15 | Cardiolipin IgM | 心肌磷脂 IGM |
JL-FA-16 | Cerebral Spinal Fluid | 腦脊髓液 |
JL-FA-17 | Chagas | 恰加斯病/南美錐蟲 |
JL-FA-18 | Chlamydia | 衣原體 |
JL-FA-19 | Chlamydia IgA | 衣原體IGA |
JL-FA-20 | Chlamydia IgG | 衣原體IGG |
JL-FA-21 | Chlamydia IgM | 衣原體IGM |
JL-FA-22 | Chlamydia Neg | 衣原體陰性 |
JL-FA-23 | Clotting Factor C3 | 凝固因子C3 |
JL-FA-24 | Clotting Factor C4 | 凝固因子C4 |
JL-FA-25 | Coccidiodes | 球孢菌 |
JL-FA-26 | Cytomegalovirus (CMV) Neg | 巨細(xì)胞病毒抗體陰性 |
JL-FA-27 | CMV IgG | 巨細(xì)胞病毒 IGG陽性 |
JL-FA-28 | CMV IgM VCA | 巨細(xì)胞病毒 IGM 陽性 |
JL-FA-29 | C-Reactive Protein (CRP) | C-反應(yīng)蛋白質(zhì) |
JL-FA-30 | Dengue Fever | 登革熱 |
JL-FA-31 | Dengue Fever IgM | 登革熱 IGM |
JL-FA-32 | DS (Double Stranded) DNA | 雙鏈脫氧核糖核酸 |
JL-FA-33 | EBNA (Epstein-Barr nuclear antigen) IgG | EB病毒核抗原 IGG |
JL-FA-34 | EBNA (Epstein-Barr nuclear antigen) IgM | EB病毒核抗原 IGM |
JL-FA-35 | Epstein Barr Virus (EBV) Negative Plasma | EB病毒陰性血漿 |
JL-FA-36 | Epstein Barr Virus (EBV) EA IgM | EB病毒早期抗原 IGM |
JL-FA-37 | Epstein Barr Virus (EBV) VCA IgM | EB病毒殼蛋白 IGM |
JL-FA-38 | Epstein Barr Virus (EBV) EA IgG | EB病毒早期抗原 IGG |
JL-FA-39 | EMA (Endomysial Antibodies) | 肌內(nèi)膜 |
JL-FA-40 | Gliadin | 麩蛋白,麥醇溶蛋白,麥膠蛋白 |
JL-FA-41 | Gliadin IgG | 麥醇溶蛋白 IGG |
JL-FA-42 | Gliadin IgA | 麥醇溶蛋白 IGA |
JL-FA-43 | Glomerular Basement Membrane (GBMA) | 腎小球基底膜病 |
JL-FA-44 | Helicobacter pylori IgA | 幽門螺旋桿菌IGA |
JL-FA-45 | Helicobacter pylori IgG | 幽門螺旋桿菌IGG |
JL-FA-46 | Helicobacter pylori IgM | 幽門螺旋桿菌IGM |
JL-FA-47 | Helicobacter pylori Negative | 幽門螺旋桿菌陰性 |
JL-FA-48 | Helicobacter pylori Positive Plasma | 幽門螺旋桿菌陰性血漿 |
JL-FA-49 | Hepatitis A Virus (HAV) Pos. Plasma | 甲型肝炎病毒陽性血漿 |
JL-FA-50 | Hepatitis A Virus (HAV) IgM | 甲型肝炎病毒IGM |
JL-FA-51 | Hepatitis B Core (HBc) IgG | 乙型肝炎病毒核心 IGG |
JL-FA-52 | Hepatitis B Core (HBc) IgM | 乙型肝炎病毒核心 IGM |
JL-FA-53 | Anti Hbe (Antibody to HBV antigen) | 乙肝抗體 |
JL-FA-54 | Hepatitis Delta Virus | 丁型肝炎病毒 |
JL-FA-55 | HBeAg (HBV e antigen) | 乙肝 E抗原 |
JL-FA-56 | anti-HBs (HBV surface antibody) | 乙肝表面抗體 |
JL-FA-57 | Hepatitis B (HBsAg) "Chronic" | 乙型肝炎（乙肝表面抗原）“慢性病 |
JL-FA-58 | HBsAg (HBV surface antigen) Serum | 乙肝表面抗原血清 |
JL-FA-59 | HBsAg (AD) | 乙肝表面抗原（AD） |
JL-FA-60 | HBsAg (AY) | 乙肝表面抗原（AY） |
JL-FA-61 | HBV Positive Plasma | 乙肝陽性血漿 |
JL-FA-62 | HBV DNA Plasma | 乙肝DNA血漿 |
JL-FA-63 | HBV DNA Serum | 乙肝DNA血清 |
JL-FA-64 | HBV DNA type A | A型 乙肝DNA |
JL-FA-65 | HBV DNA type B | B型 乙肝DNA |
JL-FA-66 | HBV DNA type C | C型 乙肝DNA |
JL-FA-67 | HBV DNA type D | D型 乙肝DNA |
JL-FA-68 | HBV DNA type E | E型 乙肝DNA |
JL-FA-69 | HBV DNA type F | F型 乙肝DNA |
JL-FA-70 | HBV Antibody HCV Antibody Plasma CO-INFECTED | 乙肝和丙肝聯(lián)合感染血漿 |
JL-FA-71 | HCV (Hepatitis C Virus) Antibody | 丙型肝炎抗體 |
JL-FA-72 | HCV Core Antigen Positive | 丙肝核心抗原 陽性 |
JL-FA-73 | HCV RNA PLASMA Genotype 1 | 基因1型丙肝RNA 血漿 |
JL-FA-74 | HCV RNA PLASMA Genotype 2 | 基因2型丙肝RNA 血漿 |
JL-FA-75 | HCV RNA PLASMA Genotype 3 | 基因3型丙肝RNA 血漿 |
JL-FA-76 | HCV RNA PLASMA Genotype 4 | 基因4型丙肝RNA 血漿 |
JL-FA-77 | HCV RNA PLASMA Genotype 5 | 基因5型丙肝RNA 血漿 |
JL-FA-78 | HCV RNA PLASMA Genotype 6 | 基因6型丙肝RNA 血漿 |
JL-FA-79 | HCV Riba single band | 丙肝免疫印跡單波段 |
JL-FA-80 | HCV RIBA Pos. (multiple bands) | 丙肝免疫印跡陽性多波段 |
JL-FA-81 | HCV Negative | 丙肝陰性 |
JL-FA-82 | HCV RNA Pos (quantitative) | 丙肝RNA陽性（定量） |
JL-FA-83 | Hepatitis E | 戊型肝炎 |
JL-FA-84 | Herpes Simplex Virus (HSV)1/2 Positive Plasma | 單純性皰疹病毒1/2陽性血漿 |
JL-FA-85 | Herpes Simplex Virus (HSV) 1 Negative Plasma | 單純性皰疹病毒1 陰性血漿 |
JL-FA-86 | Herpes Simplex Virus (HSV) 1 IgG | 單純性皰疹病毒1 IGG |
JL-FA-87 | Herpes Simplex Virus (HSV 1) IgM | 單純性皰疹病毒1 IGM |
JL-FA-88 | Herpes Simplex Virus (HSV) 2 IgG | 單純性皰疹病毒2 IGG |
JL-FA-89 | Herpes Simplex Virus (HSV) 2 IgM | 單純性皰疹病毒2 IGG |
JL-FA-90 | Histone | 組蛋白 |
JL-FA-91 | Human Anti Mouse Ab (HAMA) | 人抗鼠抗體 |
JL-FA-92 | Human immunodeficiency virus (HIV) 1 Neg | HIV I 陰性 |
JL-FA-93 | anti Human immunodeficiency virus (HIV) 1 Plasma | 抗HIV I 血漿 |
JL-FA-94 | anti Human immunodeficiency virus (HIV) 1 Serum | 抗HIV I 血清 |
JL-FA-95 | anti Human immunodeficiency virus (HIV) 2 Western Blot Tested | 抗HIV 2 免疫印跡 |
JL-FA-96 | anti Human immunodeficiency virus (HIV) 1/2 2 HIV (+) | 抗HIV 1/2 2 HIV陽性 |
JL-FA-97 | Human immunodeficiency virus (HIV) Ag | HIV抗原 |
JL-FA-98 | HIV RNA (quantitative) Plasma | HIV RNA 定量血漿 |
JL-FA-99 | HIV RNA (quantitative) Serum | HIV RNA 定量血清 |
JL-FA-100 | HIV1 Subtype A | HIV1 亞型A |
JL-FA-101 | HIV1 Subtype B | HIV1 亞型B |
JL-FA-102 | HIV1 Subtype C | HIV1 亞型C |
JL-FA-103 | HIV1 Subtype D | HIV1 亞型D |
JL-FA-104 | HIV1 Subtype E | HIV1 亞型E |
JL-FA-105 | HIV1 Subtype F | HIV1 亞型F |
JL-FA-106 | HIV1 Subtype G | HIV1 亞型G |
JL-FA-107 | HIV1 Subtype H | HIV1 亞型H |
JL-FA-108 | HIV1 Subtype J | HIV1 亞型J |
JL-FA-109 | HIV1 Subtype K | HIV1 亞型K |
JL-FA-110 | HIV1 Group O | HIV1 亞型O |
JL-FA-111 | Human immunodeficiency virus (HIV) 2 Antibody Plasma | HIV 2 抗體血漿 |
JL-FA-112 | Human immunodeficiency virus (HIV) 2 Antibody Serum | HIV 2 抗體血清 |
JL-FA-113 | HPV (Human Papiloma Virus) Negative | 人乳狀瘤病毒HPV陰性 |
JL-FA-114 | HPV (Human Papiloma Virus) Positive | 人乳狀瘤病毒HPV陽性 |
JL-FA-115 | Human immunodeficiency virus (HIV) Antibody HCV Antibody Plasma COINFECTED | HIV 抗體 HCV |
JL-FA-116 | Human T-cell Lymphotropic Virus (HTLV) I/II | 人嗜T淋巴細(xì)胞病毒(HTLV) I/II |
JL-FA-117 | Human T-cell Lymphotropic Virus (HTLV) I | 人嗜T淋巴細(xì)胞病毒(HTLV) I |
JL-FA-118 | Human T-cell Lymphotropic Virus (HTLV) II | 人嗜T淋巴細(xì)胞病毒(HTLV) II |
JL-FA-119 | Jo-1 | 多發(fā)性肌炎抗原JO-1 |
JL-FA-120 | IgE < 5,000 Ku/L | IgE < 5,000 Ku/L |
JL-FA-121 | Legionella | 軍團桿菌屬 |
JL-FA-122 | Leptospira | 軍團桿菌屬 |
JL-FA-123 | Lyme Disease | 萊姆(氏)病:蜱傳播的全身性疾病,常在夏季發(fā)生 |
JL-FA-124 | Lyme IgG | 萊姆(氏)病 IGG |
JL-FA-125 | Lyme IgM | 萊姆(氏)病 IGM |
JL-FA-126 | Lyme Disease Neg | 萊姆(氏)病 陰性 |
JL-FA-127 | Malaria | 瘧疾 |
JL-FA-128 | Mononucleosis (infectious) | 單核細(xì)胞增多癥（有傳染性的） |
JL-FA-129 | Mononucleosis Negative | 單核細(xì)胞增多癥陰性 |
JL-FA-130 | Measles Negative | 麻疹 陰性 |
JL-FA-131 | Measles IgG | 麻疹 IGG |
JL-FA-132 | Measles IgM | 麻疹 IGM |
JL-FA-133 | Microsomal Anti-thyroid peroxidase antibody (TPO) Positive Plasma Standard Titer (typically 1,000-3,000 IU/mL) | 微粒體抗甲狀腺過氧化物酶抗體 |
JL-FA-134 | Microsomal Anti-thyroid peroxidase antibody (TPO) Negative Plasma | 微粒體抗甲狀腺過氧化物酶抗體 |
JL-FA-135 | Anti-mitochondrial antibody (AMA) | 抗線粒體抗體 |
JL-FA-136 | Multiple Sclerosis | 多發(fā)性硬化癥 |
JL-FA-137 | Mumps IgG | 流行性腮腺炎 IGG |
JL-FA-138 | Mumps Ab IgM | 流行性腮腺炎抗體 IGM |
JL-FA-139 | Mumps Antibody Negative Plasma | 流行性腮腺炎抗體陰性血漿 |
JL-FA-140 | Mumps Antibody Negative Serum | 流行性腮腺炎抗體陰性血清 |
JL-FA-141 | Myeloma Plasma | 骨髓瘤血漿 |
JL-FA-142 | Myeloma IgA | 骨髓瘤IGA |
JL-FA-143 | Myeloma IgE | 骨髓瘤IGE |
JL-FA-144 | Myeloma IgG | 骨髓瘤IGG |
JL-FA-145 | Myeloma IgM | 骨髓瘤IGM |
JL-FA-146 | Mycoplasma | 支原體 |
JL-FA-147 | Mycoplasma Negative | 支原體陰性 |
JL-FA-148 | Mycoplasma IgG | 支原體IGG |
JL-FA-149 | Mycoplasma IgM | 支原體IGM |
JL-FA-150 | Mycoplasma PCR | 支原體PCR |
JL-FA-151 | Normal Human Plasma | 正常人血漿 |
JL-FA-152 | Normal Human Serum | 正常人血清 |
JL-FA-153 | Nuclear Antibody Centromere | 核抗體著絲粒 |
JL-FA-154 | Nuclear Antibody, Speckled ANA | 核抗體，斑點抗核抗體 |
JL-FA-155 | Nuclear Antibody, Nucleolar ANA | 核抗體,核仁抗核抗體 |
JL-FA-156 | Nuclear Antibody, Homogeneous ANA | 核抗體，同質(zhì)抗核抗體 |
JL-FA-157 | Nuclear Antiobody, Speckled. (ANA) Negative | 核抗體，斑點?？购丝贵w陰性 |
JL-FA-158 | P-ANCA (associated neutrophil cytoplasmic antibodies) | 相關(guān)的嗜中性粒細(xì)胞胞漿抗體 |
JL-FA-159 | Parietal Cell Antibody (PCA) | 胃)壁細(xì)胞抗體 |
JL-FA-160 | Parvo positive plasma | 細(xì)小病毒陽性血漿 |
JL-FA-161 | Parvo IgM | 細(xì)小病毒 IGM |
JL-FA-162 | Parvo IgG | 細(xì)小病毒 IGG |
JL-FA-163 | Parvo Negative Plasma | 細(xì)小病毒陰性血漿 |
JL-FA-164 | Parvo DNA positive | 細(xì)小病毒 DNA 陽性 |
JL-FA-165 | Phospholipid Positive Plasma | 磷脂陽性血漿 |
JL-FA-166 | Prothrombin | 凝血酶原,凝血因子 |
JL-FA-167 | Rheumatoid Factor (RF) <1000 IU/mL | 類風(fēng)濕因子<1000 IU/mL |
JL-FA-168 | Rheumatoid Factor (RF) 1001-2000 IU/mL | 類風(fēng)濕因子1001-2000 IU/mL |
JL-FA-169 | Rheumatoid Factor (RF) 2001-4000 IU/mL | 類風(fēng)濕因子 2001-4000 IU/mL |
JL-FA-170 | Rheumatoid Factor (RF) 4001-5000 IU/mL | 類風(fēng)濕因子 4001-5000 IU/mL |
JL-FA-171 | Rheumatoid Factor (RF) >5000 IU/mL | 類風(fēng)濕因子>5000 IU/mL |
JL-FA-172 | Ribonucleoprotein (RNP) Positive | 核糖核蛋白陽性 |
JL-FA-173 | Rubella Chimeric | 風(fēng)疹 |
JL-FA-174 | Rubella Negative | 風(fēng)疹陰性 |
JL-FA-175 | Rubella IgG | 風(fēng)疹I(lǐng)GG |
JL-FA-176 | Rubella IgM | 風(fēng)疹I(lǐng)GM |
JL-FA-177 | Rubeola Negative Plasma | 風(fēng)疹陰性血漿 |
JL-FA-178 | Rubeola IgG | 風(fēng)疹I(lǐng)GG |
JL-FA-179 | Scleroderma (Scl-70) Pos | 膠原沉著病,硬皮病,硬皮癥 陽性 |
JL-FA-180 | Scleroderma (Scl-70) Negative | 硬皮病陰性 |
JL-FA-181 | Sickle Cell Fresh Whole Blood | 鐮刀形紅細(xì)胞新鮮全血 |
JL-FA-182 | Smith (SM) | 抗Smith抗體陽性血清（SLE的特征性抗體） |
JL-FA-183 | SMITH RNP | 抗RNP抗體陽性血清（SLE的特征性抗體） |
JL-FA-184 | Smooth Muscle (ASMA) | 抗平滑肌抗體陽性血清 |
JL-FA-185 | Sjogren syndrome antigen A (SSA) Positive | 舍格倫綜合征或干燥綜合征抗原A 陽性 |
JL-FA-186 | Sjogren syndrome antigen B (SSB) Positive | 舍格倫綜合征抗原B 陽性 |
JL-FA-187 | Sjogren syndrome antigen B (SSB) Negative | 舍格倫綜合征抗原B陰性 |
JL-FA-188 | Streptolysin O Ab (ASO) | 鏈球菌溶血素O抗體 |
JL-FA-189 | Syphilis (RPR - Rapid Plasma Reagin) Positive Plasma | 梅毒（梅毒-快速血漿反應(yīng)）陽性血漿 |
JL-FA-190 | Syphilis (RPR - Rapid Plasma Reagin) Negative Plasma | 梅毒（梅毒-快速血漿反應(yīng)）陰性血漿 |
JL-FA-191 | Syphilis/ATA/T. pallidum IgG | 梅毒ATA/T，蒼白球IGG |
JL-FA-192 | Syphilis/ATA/T. pallidum IgM | 梅毒ATA/T，蒼白球IGM |
JL-FA-193 | Systemic Lupus Erythematosus (SLE) Positive | 全身性紅斑狼瘡陽性 |
JL-FA-194 | Systemic Lupus Erythematosus (SLE) Negative | 全身性紅斑狼瘡陰性 |
JL-FA-195 | TG/TPO Positive (Standard Titer 1,000 - 3000 IU/mL) | 甲狀腺球蛋白/甲狀腺過氧化物酶陽性 |
JL-FA-196 | TG/TPO Negative | 甲狀腺球蛋白/甲狀腺過氧化物酶陰性 |
JL-FA-197 | TTG (Tissue Transglutaminase) | 組織轉(zhuǎn)谷氨酰胺酶 |
JL-FA-198 | TTG (Tissue Transglutaminase) IgA | 組織轉(zhuǎn)谷氨酰胺酶 IGA |
JL-FA-199 | ToRCH (Toxo, Rubella, CMV, HSV) Positive | 優(yōu)生優(yōu)育（弓形蟲，風(fēng)疹，巨細(xì)胞，單胞）陽性 |
JL-FA-200 | ToRCH (Toxo, Rubella, CMV, HSV) Negative | 優(yōu)生優(yōu)育（弓形蟲，風(fēng)疹，巨細(xì)胞，單胞）陰性 |
JL-FA-201 | Toxoplasmosis (Toxo) | 弓形蟲病 |
JL-FA-202 | Toxoplasmosis (Toxo) IgG | 弓形蟲病IGG |
JL-FA-203 | Toxoplasmosis (Toxo) IgM | 弓形蟲病IGM |
JL-FA-204 | Thyroglobulin (TG) Positive Plasma | 甲狀腺球蛋白陽性血漿 |
JL-FA-205 | Thyroglobulin (TG) Negative | 甲狀腺球蛋白陰性 |
JL-FA-206 | Varicella-Zoster Virus (VZV) Negative | 水痘-帶狀皰疹病毒陰性 |
JL-FA-207 | Varicella-Zoster Virus (VZV) IgG | 水痘-帶狀皰疹病毒IGG |
JL-FA-208 | Varicella-Zoster Virus (VZV) IgM | 水痘-帶狀皰疹病毒IGM |
JL-FA-209 | West Nile Virus (WNV) | 西尼羅河腦炎病毒 |
JL-FA-210 | West Nile Virus (WNV) IgM | 西尼羅河腦炎病毒IGM |
美國
干擾素偽裝免疫細(xì)胞
免疫生物學(xué)教授Annette Oxenius的研究小組現(xiàn)在發(fā)現(xiàn)，是什么阻止nk細(xì)胞殺死免疫系統(tǒng)的“來自于其他部門的同事”：健康CD8 +T細(xì)胞能夠檢測免疫信使物質(zhì)1型干擾素，1型干擾素通過與這些免疫細(xì)胞的特定表面受體結(jié)合，從而隱藏它們的應(yīng)激。換句話說，1型干擾素作為一種偽裝斗篷使得免疫細(xì)胞不被NK細(xì)胞看見。如果T細(xì)胞缺乏1型干擾素的停泊位點，那么它們就會被NK細(xì)胞追殺直至滅絕。
使用感染兩種模型病毒的小鼠，研究人員發(fā)現(xiàn)，如果動物的CD8 +t細(xì)胞缺乏這些干擾素的受體，不僅NK細(xì)胞消除感染病毒的細(xì)胞，而且免疫細(xì)胞也被認(rèn)為采取了行動，從而削弱了抗病毒的免疫反應(yīng)。
訓(xùn)練有素的細(xì)胞死亡信號
研究人員使用CD8 + T細(xì)胞沒有任何1型干擾素受體的小鼠探索工作機制是如何運作的，以及缺乏1型干擾素的CD8 + T細(xì)胞是如何耗盡NK細(xì)胞的。如果沒有自然殺手的存在，盡管缺乏干擾素檢測，但T細(xì)胞依然會增多，成熟和發(fā)育。此外，瑞士蘇黎世聯(lián)邦理工學(xué)院的免疫生物學(xué)家發(fā)現(xiàn)，這些無需傳感器的T細(xì)胞逐漸形成其表面的“識別標(biāo)簽”，一旦與NK細(xì)胞接觸，就會引發(fā)NK細(xì)胞的殺傷作用。因此，這些“應(yīng)激標(biāo)簽”的表達通過干擾素結(jié)合以及通過T細(xì)胞上的干擾素受體發(fā)出信號被抑制。如果由于受體的缺乏而阻止了信號的傳輸，那么細(xì)胞會大量表達這些應(yīng)激分子。
自身免疫性疾病的機制?
到目前為止，尚不清楚人類是否具有相同的機制。然而，人類免疫系統(tǒng)用來保護T細(xì)胞避免NK細(xì)胞攻擊的基本過程很可能是類似的。在一方面，研究人員現(xiàn)在揭示應(yīng)激T細(xì)胞需要保護自己免受NK細(xì)胞攻擊的機制。另一方面，這項發(fā)現(xiàn)形成了新的假設(shè)。例如，可以想到的是，缺乏干擾素受體的T細(xì)胞活化顯示出它們?yōu)?ldquo;應(yīng)激的”，并因此殺死了。自身免疫反應(yīng)性T細(xì)胞的活化過程中可能會出現(xiàn)這樣的情況，例如，它通常發(fā)生在不存在高濃度的1型干擾素。Oxenius和她的團隊有很濃厚的興趣將在未來幾年內(nèi)測試這些令人興奮的假設(shè)。
加州大學(xué)圣地亞哥分校的生物學(xué)家發(fā)現(xiàn)能夠使動物細(xì)胞產(chǎn)生核糖體的化學(xué)系統(tǒng)中的‘未知環(huán)節(jié)’——每個細(xì)胞中含有數(shù)千蛋白‘工廠’加工所有建立組織和維持生命所必須的蛋白。他們的發(fā)現(xiàn)不僅強迫分子生物學(xué)基礎(chǔ)教科書的修訂，而且也為科學(xué)家提供較好的理解如何限制自由的細(xì)胞生長，如癌癥，也許通過控制核糖體的輸出來調(diào)節(jié)。這一研究發(fā)現(xiàn)發(fā)表在6月23日的《Genes & Development》期刊上。
美國
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二維碼掃一掃
【公司名稱】 廣州健侖生物科技有限公司
【】 楊永漢
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【騰訊 】 2042552662
【公司地址】 廣州清華科技園創(chuàng)新基地番禺石樓鎮(zhèn)創(chuàng)啟路63號二期2幢101-3室
【企業(yè)文化】
Interferon disguises immune cells
Annette Oxenius' team of immunobiology professors now finds out what "colleagues from other departments" are preventing nk cells from killing the immune system: Healthy CD8 + T cells are able to detect immunocompetent substances Type 1 interferon, type 1 interferon By binding to specific surface receptors of these immune cells, their stress is hidden. In other words, type 1 interferons act as a camouflage cape so that immune cells are not seen by NK cells. If T cells lack type 1 interferon docking sites, they are killed by NK cells until they become extinct.
Using mice infected with both model viruses, the researchers found that if the animal's CD8 + T cells lacked these interferon receptors, not only did NK cells eliminate the virus-infected cells, but immune cells were also thought to have taken action that weakened Antiviral immune response.
Trained cell death signal
Researchers using mice that did not have any Type 1 interferon receptor on CD8 + T cells explored how the working mechanism works and how NK cells are depleted by CD8 + T cells lacking type 1 interferon. Without the existence of a natural killer, T-cells will continue to proliferate, mature, and develop despite the lack of interferon testing. In addition, immune biologists at the Federal Institute of Technology in Zurich, Switzerland, found that these sensorless T cells evolved to form "labels" on their surface that, when contacted with NK cells, elicited NK cell killing. Thus, the expression of these "stress tags" is inhibited by interferon binding as well as signaling by interferon receptors on T cells. If signaling is blocked because of lack of receptors, the cells express large quantities of these stressors.
Mechanisms of autoimmune diseases?
So far, it is unclear whether human beings have the same mechanism. However, the basic process that the human immune system uses to protect T cells from NK cell challenge is likely to be similar. On the one hand, researchers now reveal that stressed T cells need a mechanism to protect themselves from attack by NK cells. On the other hand, this finding has led to new assumptions. For example, it is conceivable that T-cell activation, which lacks interferon receptors, shows that they are "stressed" and therefore killed. This may occur during the activation of autoimmune reactive T cells, for example, it typically occurs in the absence of high concentrations of type 1 interferons. Oxenius and her team are very interested in testing these exciting assumptions in the coming years.
Biologists at the University of California, San Diego discovered the 'unknown' part of the chemical system that produces ribosomes in animal cells - thousands of proteins in each cell. The 'factory' processes all the proteins necessary to build and sustain life. Their findings not only force the revision of basic textbooks in molecular biology, but also provide scientists with a better understanding of how to limit free cell growth, such as cancer, perhaps by controlling ribosomal output. The study was published in the June 23 issue of Genes & Development.
