WordNet

a leukocyte readily stained with eosin (同)eosinophile
of or relating to eosinophil

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/03/10 05:28:10」(JST)

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3D Rendering of Eosinophil

Eosinophil granulocytes, usually called eosinophils or eosinophiles (or, less commonly, acidophils), are white blood cells and one of the immune system components responsible for combating multicellular parasites and certain infections in vertebrates. Along with mast cells, they also control mechanisms associated with allergy and asthma. They are granulocytes that develop during hematopoiesis in the bone marrow before migrating into blood.

These cells are eosinophilic or 'acid-loving' as shown by their affinity to coal tar dyes: Normally transparent, it is this affinity that causes them to appear brick-red after staining with eosin, a red dye, using the Romanowsky method. The staining is concentrated in small granules within the cellular cytoplasm, which contain many chemical mediators, such as histamines and proteins such as eosinophil peroxidase, ribonuclease (RNase), deoxyribonucleases, lipase, plasminogen, and major basic protein. These mediators are released by a process called degranulation following activation of the eosinophil, and are toxic to both parasite and host tissues.

In normal individuals, eosinophils make up about 1-6% of white blood cells, and are about 12-17 micrometers in size.^[1] They are found in the medulla and the junction between the cortex and medulla of the thymus, and, in the lower gastrointestinal tract, ovary, uterus, spleen, and lymph nodes, but not in the lung, skin, esophagus, or some other internal organs^[vague] under normal conditions. The presence of eosinophils in these latter organs is associated with disease. Eosinophils persist in the circulation for 8–12 hours, and can survive in tissue for an additional 8–12 days in the absence of stimulation.^[2] Pioneering work in the 1980s elucidated that eosinophils were unique granulocytes, having the capacity to survive for extended periods of time after their maturation as demonstrated by ex-vivo culture experiments.

Eosinophil development, migration and activation

Eosinophils develop and mature in the bone marrow. They differentiate from myeloid precursor cells in response to the cytokines interleukin 3 (IL-3), interleukin 5 (IL-5), and granulocyte macrophage-colony stimulating factor (GM-CSF).^[3]^[4]^[5] Eosinophils produce and store many secondary granule proteins prior to their exit from the bone marrow. After maturation, eosinophils circulate in blood and migrate to inflammatory sites in tissues, or to sites of helminth infection in response to chemokines like CCL11 (eotaxin-1), CCL24 (eotaxin-2), CCL5 (RANTES), 5-hydroxyicosatetraenoic acid and 5-oxo-eicosatetraenoic acid, and certain leukotrienes like leukotriene B4 (LTB4) and MCP1/4. At these infectious sites, eosinophils are activated by Type 2 cytokines released from a specific subset of helper T cells (T_h2); IL-5, GM-CSF, and IL-3 are important for eosinophil activation as well as maturation. There is evidence to suggest that eosinophil granule protein expression is regulated by the non-coding RNA EGOT (gene)^[6]

Functions of eosinophils

Following activation, eosinophils effector functions include production of:

cationic granule proteins and their release by degranulation.^[7]^[8]^[9]
reactive oxygen species such as hypobromite, superoxide, and peroxide (hypobromous acid, which is preferentially produced by eosinophil peroxidase).^[10]
lipid mediators like the eicosanoids from the leukotriene (e.g., LTC₄, LTD₄, LTE₄) and prostaglandin (e.g., PGE₂) families.^[11]
enzymes, such as elastase.
growth factors such as TGF beta, VEGF, and PDGF.^[12]^[13]
cytokines such as IL-1, IL-2, IL-4, IL-5, IL-6, IL-8, IL-13, and TNF alpha.^[14]^[8]

In addition, there are also eosinophils that play a role in fighting viral infections, which is evident from the abundance of RNases they contain within their granules, and in fibrin removal during inflammation. Eosinophils along with basophils and mast cells, are important mediators of allergic responses and asthma pathogenesis and are associated with disease severity. They also fight helminth (worm) colonization and may be slightly elevated in the presence of certain parasites. Eosinophils are also involved in many other biological processes, including postpubertal mammary gland development, oestrus cycling, allograft rejection and neoplasia.^[14] They have also recently been implicated in antigen presentation to T cells.^[15]

Eosinophil granule proteins

Following activation by an immune stimulus, eosinophils degranulate to release an array of cytotoxic granule cationic proteins that are capable of inducing tissue damage and dysfunction.^[16] These include:

major basic protein (MBP)
eosinophil cationic protein (ECP)
eosinophil peroxidase (EPO)
eosinophil-derived neurotoxin (EDN)

Major basic protein, eosinophil peroxidase, and eosinophil cationic protein are toxic to many tissues.^[14] Eosinophil cationic protein and eosinophil-derived neurotoxin are ribonucleases with antiviral activity.^[17] Major basic protein induces mast cell and basophil degranulation, and is implicated in peripheral nerve remodelling.^[18]^[19] Eosinophil cationic protein creates toxic pores in the membranes of target cells allowing potential entry of other cytotoxic molecules to the cell,^[20] can inhibit proliferation of T cells, suppress antibody production by B cells, induce degranulation by mast cells, and stimulate fibroblast cells to secrete mucus and glycosaminoglycan.^[21] Eosinophil peroxidase forms reactive oxygen species and reactive nitrogen intermediates that promote oxidative stress in the target, causing cell death by apoptosis and necrosis.^[14]

Eosinophilia

An increase in eosinophils, i.e., the presence of more than 500 eosinophils/microlitre of blood is called an eosinophilia, and is typically seen in people with a parasitic infestation of the intestines, collagen vascular disease (such as rheumatoid arthritis), malignant diseases such as Hodgkin's disease, extensive skin diseases (such as exfoliative dermatitis), Addison's disease, reflux esophagitis (in which eosinophils will be found in the squamous epithelium of the esophagus), eosinophilic esophagitis, and with the use of certain drugs such as penicillin. But, perhaps the most common cause for eosinophilia is an allergic condition such as asthma. In 1989, contaminated L-tryptophan supplements caused a deadly form of eosinophilia known as eosinophilia-myalgia syndrome, which was reminiscent of the Toxic Oil Syndrome in Spain in 1981.

Reference ranges for blood tests of white blood cells, comparing eosinophil granulocyte amount (shown in light red) with other cells.

Treatment

Treatments used to combat autoimmune diseases and conditions caused by eosinophils include:

corticosteroids- promote apoptosis. Numbers of eosinophils in blood are rapidly reduced
monoclonal antibody therapy- e.g., mepolizumab or reslizumab against IL-5, prevents eosinophilopoiesis
antagonists of leukotriene synthesis or receptors
Gleevec (STI571)- inhibits PDGF-BB in hypereosinophilic leukemia

Additional images

Eosinophil in peripheral blood (Giemsa stain)
Blood cell lineage
Eosinophil

References

^ Young, Barbara; Lowe, joseph o'connell; Stevens, Alan; Heath, John W. (2006). Wheater's Functional Histology (5 ed.). Elsevier Limited. ISBN 0-443-06850-X.
^ Young, Barbara; Lowe, James S.; Stevens, Alan; Heath, John W. (2006). Wheater's Functional Histology (5 ed.). Elsevier Limited. ISBN 0-443-06850-X.
^ Metcalf D, Begley C, Nicola N, Johnson G (1987). "Quantitative responsiveness of murine hemopoietic populations in vitro and in vivo to recombinant multi-CSF (IL-3)". Exp Hematol 15 (3): 288–95. PMID 3493174.
^ Metcalf D, Burgess A, Johnson G, Nicola N, Nice E, DeLamarter J, Thatcher D, Mermod J (1986). "In vitro actions on hemopoietic cells of recombinant murine GM-CSF purified after production in Escherichia coli: comparison with purified native GM-CSF". J Cell Physiol 128 (3): 421–31. doi:10.1002/jcp.1041280311. PMID 3528176.
^ Yamaguchi Y, Suda T, Suda J, Eguchi M, Miura Y, Harada N, Tominaga A, Takatsu K (1988). "Purified interleukin 5 supports the terminal differentiation and proliferation of murine eosinophilic precursors". J Exp Med 167 (1): 43–56. doi:10.1084/jem.167.1.43. PMC 2188821. PMID 3257253.
^ Wagner LA, Christensen CJ, Dunn DM, et al. (June 2007). "EGO, a novel, noncoding RNA gene, regulates eosinophil granule protein transcript expression". Blood 109 (12): 5191–8. doi:10.1182/blood-2006-06-027987. PMC 1890841. PMID 17351112.
^ Trulson A, Byström J, Engström A, Larsson R, Venge P (2007). "The functional heterogeneity of eosinophil cationic protein is determined by a gene polymorphism and post-translational modifications". Clin Exp Allergy 37 (2): 208–18. doi:10.1111/j.1365-2222.2007.02644.x. PMID 17250693.
^ ^a ^b Hogan S, Rosenberg H, Moqbel R, Phipps S, Foster PS, Lacy P, Kay AB, Rothenberg ME (2008). "Eosinophils: Biological Properties and Role in Health and Disease". Clin Exp Allergy 38 (5): 709–50. doi:10.1111/j.1365-2222.2008.02958.x. PMC 3406327. PMID 20421642.
^ Lacy P (2005). "The role of Rho GTPases and SNAREs in mediator release from granulocytes". Pharmacol Ther 107 (3): 358–76. doi:10.1016/j.pharmthera.2005.03.008. PMID 15951020.
^ Saito K, Nagata M, Kikuchi I, Sakamoto Y (2004). "Leukotriene D4 and eosinophil transendothelial migration, superoxide generation, and degranulation via beta2 integrin". Ann Allergy Asthma Immunol 93 (6): 594–600. doi:10.1016/S1081-1206(10)61269-0. PMID 15609771.
^ Bandeira-Melo C, Bozza P, Weller P (2002). "The cellular biology of eosinophil eicosanoid formation and function". J Allergy Clin Immunol 109 (3): 393–400. doi:10.1067/mai.2002.121529. PMID 11897981.
^ Kato Y, Fujisawa T, Nishimori H, Katsumata H, Atsuta J, Iguchi K, Kamiya H (2005). "Leukotriene D4 induces production of transforming growth factor-beta1 by eosinophils". Int Arch Allergy Immunol. 137. Suppl 1 (1): 17–20. doi:10.1159/000085427. PMID 15947480.
^ Horiuchi T, Weller P (1997). "Expression of vascular endothelial growth factor by human eosinophils: upregulation by granulocyte macrophage colony-stimulating factor and interleukin-5". Am J Respir Cell Mol Biol 17 (1): 70–7. doi:10.1165/ajrcmb.17.1.2796. PMID 9224211.
^ ^a ^b ^c ^d Rothenberg M, Hogan S (2006). "The eosinophil". Annu Rev Immunol 24 (1): 147–74. doi:10.1146/annurev.immunol.24.021605.090720. PMID 16551246.
^ Shi H (2004). "Eosinophils function as antigen-presenting cells". J Leukoc Biol 76 (3): 520–7. doi:10.1189/jlb.0404228. PMID 15218055.
^ Gleich G, Adolphson C (1986). "The eosinophilic leukocyte: structure and function". Adv Immunol 39: 177–253. doi:10.1016/S0065-2776(08)60351-X. PMID 3538819.
^ Slifman N, Loegering D, McKean D, Gleich G (1986). "Ribonuclease activity associated with human eosinophil-derived neurotoxin and eosinophil cationic protein". J Immunol 137 (9): 2913–7. PMID 3760576.
^ Zheutlin L, Ackerman S, Gleich G, Thomas L (1984). "Stimulation of basophil and rat mast cell histamine release by eosinophil granule-derived cationic proteins". J Immunol 133 (4): 2180–5. PMID 6206154.
^ Morgan R, Costello R, Durcan N, Kingham P, Gleich G, McLean W, Walsh M (2005). "Diverse effects of eosinophil cationic granule proteins on IMR-32 nerve cell signaling and survival". Am J Respir Cell Mol Biol 33 (2): 169–77. doi:10.1165/rcmb.2005-0056OC. PMID 15860794.
^ Young J, Peterson C, Venge P, Cohn Z (1986). "Mechanism of membrane damage mediated by human eosinophil cationic protein". Nature 321 (6070): 613–6. doi:10.1038/321613a0. PMID 2423882.
^ Venge P, Byström J, Carlson M, Hâkansson L, Karawacjzyk M, Peterson C, Sevéus L, Trulson A (1999). "Eosinophil cationic protein (ECP): molecular and biological properties and the use of ECP as a marker of eosinophil activation in disease". Clin Exp Allergy 29 (9): 1172–86. doi:10.1046/j.1365-2222.1999.00542.x. PMID 10469025.

External links

eosinophilic+leukocyte at eMedicine Dictionary
Bioweb at UWLAX Eosinophil
Histology at ucsf.edu
"What is an eosinophil?" at the Cincinnati Center for Eosinophilic Disorders

UpToDate Contents

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1. 原因不明の好酸球増加症患者に対するアプローチ approach to the patient with unexplained eosinophilia
2. 好酸球の生物学および好酸球増多症の原因 eosinophil biology and causes of eosinophilia
3. Hypereosinophilic syndromes: Clinical manifestations, pathophysiology, and diagnosis
4. Allergic fungal rhinosinusitis
5. 末梢血塗抹標本の評価 evaluation of the peripheral blood smear

English Journal

Lycopene treatment prevents hematological, reproductive and histopathological damage induced by acute zearalenone administration in male Swiss mice.

Boeira SP1, Filho CB2, Del'fabbro L2, Roman SS3, Royes LF4, Fighera MR5, Jessé CR6, Oliveira MS1, Furian AF7.Author information 1Programa de Pós-Graduação em Farmacologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil.2Universidade Federal do Pampa, Campus Itaqui, 97650-000 Itaqui, RS, Brazil.3Universidade Regional Integrada do Alto Uruguai e das Missões, Campus de Erechim, 99700-000 Erechim, RS, Brazil.4Programa de Pós-Graduação em Farmacologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil; Departamento de Educação Física e Desportos, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil.5Programa de Pós-Graduação em Farmacologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil; Departamento de Neuropsiquiatria, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil.6Universidade Federal do Pampa, Campus Itaqui, 97650-000 Itaqui, RS, Brazil; Programa de Pós-Graduação em Bioquímica, Universidade Federal do Pampa, 97500-970 Uruguaiana, RS, Brazil.7Programa de Pós-Graduação em Farmacologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil; Departamento de Tecnologia e Ciência dos Alimentos, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. Electronic address: furian.anaflavia@gmail.com.AbstractZearalenone (ZEA) is a mycotoxin commonly found as a contaminant in cereals. ZEA toxicity targets mainly the reproductive system, and oxidative stress plays an etiological role in its toxic effects. Therefore, the present study aimed to investigate the effect of lycopene, a potent carotenoid antioxidant, on markers of oxidative stress in liver, kidney and testes, and on reproductive, hematological and histopathological parameters after ZEA administration. Adult Swiss albino male mice received lycopene (20mg/kg, p.o.) for ten days before a single oral administration of ZEA (40mg/kg, p.o.), and 48h thereafter tissues (liver, kidney, testes and blood) were collected for biochemical, hematological and histological analyses. Lycopene prevented ZEA-induced changes in hematological parameters (increased number of leukocytes, segmented neutrophils, sticks, eosinophils and monocytes and decreased number of red blood cells (RBC), number of lymphocytes and platelets). Moreover, lycopene prevented the reduction in the number and motility of spermatozoa and the testicular tissue damage induced by ZEA. In addition, lycopene prevented the decrease in glutathione-S-transferase activity in kidney and testes and increased glutathione-S-transferase activity per se in the liver, kidneys and testes as well as superoxide dismutase activity in the liver. In summary, lycopene was able to prevent ZEA-induced acute toxic effects in male mice, suggesting that this antioxidant carotenoid may represent a promising prophylactic strategy against ZEA toxicity.
Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie.Exp Toxicol Pathol.2014 Jul;66(4):179-85. doi: 10.1016/j.etp.2014.01.002. Epub 2014 Feb 3.
Zearalenone (ZEA) is a mycotoxin commonly found as a contaminant in cereals. ZEA toxicity targets mainly the reproductive system, and oxidative stress plays an etiological role in its toxic effects. Therefore, the present study aimed to investigate the effect of lycopene, a potent carotenoid antioxi
PMID 24503513

Resolvin E1 promotes resolution of inflammation in a mouse model of an acute exacerbation of allergic asthma.

Flesher RP, Herbert C, Kumar RK.Author information *Inflammation and Infection Research Centre, School of Medical Sciences, University of New South Wales, Sydney, NSW 2052, Australia.AbstractEndogenous mediators, such as RvE1 (resolvin E1), promote resolution of an inflammatory response and have potential as novel therapeutic agents. In the present study, we investigated the activity of RvE1 in a model of an acute exacerbation of chronic allergic asthma in mice. Animals sensitized to OVA (ovalbumin) received controlled low-level challenge with aerosolized antigen for 4 weeks, followed by a single moderate-level challenge to simulate an allergen-induced exacerbation of asthmatic inflammation. Induction of an exacerbation was associated with rapid recruitment of neutrophils, lymphocytes and eosinophils, together with increased levels of Th2 and pro-inflammatory cytokines. When administered before the final moderate-level challenge, RvE1 had only a modest effect on airway inflammation. To assess its effects when administered after induction of an exacerbation, we first characterized the cellular and molecular events associated with spontaneous resolution of airway inflammation over the following 96 h. Subsequently, we showed that administration of RvE1 at 2 and 8 h after the final challenge accelerated this process significantly. Specifically, RvE1 promoted a decline in the number of inflammatory cells, concentration of cytokines in lavage fluid and expression of mRNA for cytokines by macrophages, confirming its pro-resolution activity. In vitro, RvE1 had no apparent effect on lymphocytes, but suppressed significantly cytokine production by pulmonary macrophages, with evidence of down-regulation of the nuclear translocation of NF-κB (nuclear factor κB) p65 in these cells. The present study provides novel evidence that RvE1 can facilitate resolution of airway inflammation in a clinically relevant model of an acute exacerbation of asthma, possibly via its effects on activated pulmonary macrophages.
Clinical science (London, England : 1979).Clin Sci (Lond).2014 Jun;126(11):805-14. doi: 10.1042/CS20130623.
Endogenous mediators, such as RvE1 (resolvin E1), promote resolution of an inflammatory response and have potential as novel therapeutic agents. In the present study, we investigated the activity of RvE1 in a model of an acute exacerbation of chronic allergic asthma in mice. Animals sensitized to OV
PMID 24344649

Aspirin Desensitization: Useful Treatment for Chronic Rhinosinusitis with Nasal Polyps (CRSwNP) in Aspirin-Exacerbated Respiratory Disease (AERD)?

Klimek L1, Dollner R, Pfaar O, Mullol J.Author information 1Center for Rhinology and Allergology, An den Quellen 10, 65183, Wiesbaden, Germany, Ludger.Klimek@Allergiezentrum.org.AbstractAspirin intolerance syndrome is due to disturbances in the arachidonic acid metabolism implicating both the lipoxygenase and cyclooxygenase pathways. This results in imbalances of eicosanoid, leukotriene and prostaglandin synthesis. Thus, preinflammatory cysteinyl leukotrienes increase and antiinflammatory prostaglandins (PG) such as PGE2 decrease. Clinically, intolerance reactions to nonsteroidal antiinflammatory drugs (NSAIDs) can lead to different clinical manifestations; five phenotypes of the aspirin intolerance syndrome are listed in the ENDA classification. Aspirin-exacerbated respiratory disease (AERD) is the most common phenotype characterized by an eosinophil-dominated inflammatory disease of the airways that presents clinically with nasal polyps, chronic sinusitis and bronchial asthma. About 34 % of patients with aspirin-induced asthma and rhinosinusitis are thought to have AERD. Important biochemical findings in many AERD patients are increased basal leukotriene levels (at least in cell cultures) that excessively increase after intake of COX-1 inhibitors. Aspirin desensitization uses the repetitive application of aspirin to induce a tolerance to NSAIDs, especially COX-1 inhibitors. After a dose-increase phase reaching a threshold dose, a dose-continuation phase is performed. For application, the nasal, bronchial, oral and intravenous routes have been described. Aspirin desensitization has been proven to be efficacious and safe and was able to reduce the need for other medications in AERD patients.
Current allergy and asthma reports.Curr Allergy Asthma Rep.2014 Jun;14(6):441. doi: 10.1007/s11882-014-0441-9.
Aspirin intolerance syndrome is due to disturbances in the arachidonic acid metabolism implicating both the lipoxygenase and cyclooxygenase pathways. This results in imbalances of eicosanoid, leukotriene and prostaglandin synthesis. Thus, preinflammatory cysteinyl leukotrienes increase and antiinfla
PMID 24682773

Japanese Journal

診断のコツ : COPDから考える (特集今ACOSを考える)

呼吸器内科 = Respiratory medicine 28(4), 289-296, 2015-10
NAID 40020638023

A novel in-frame deletion in the leucine zipper domain of C/EBPε leads to neutrophil-specific granule deficiency

Journal of Immunology 195(1), 80-86, 2015-07-01
NAID 120005647665

好酸球性食道炎 (特集酸関連疾患 : 最新の診断・治療動向) -- (特論)

日本臨床 73(7), 1221-1226, 2015-07
NAID 40020512369

Related Pictures

★リンクテーブル★

リンク元	「好酸球」「造血幹細胞」「eosinophilic」「acidophile」
拡張検索	「acute eosinophilic pneumonia」「eosinophil granule protein」「eosinophilic endomyocardial disease」「eosinophilic pustular dermatosis」

「好酸球」

Eosinophil granulocyte
	Eosinophil under the microscope (400x) from a peripheral blood smear. Red blood cells surround the eosinophil, two platelets at the top left corner.
Identifiers
Code	TH H2.00.04.1.02017
	Anatomical terminology

　　[★]

英: eosinophil (Z), eosinophile
関: 顆粒球、白血球、好塩基球

白血球

顆粒球

組織学

酸性色素(エオシン)で染まる顆粒(好酸性顆粒)を持つ　→　ギムザ染色で赤っぽい顆粒がみえる (HIS.190 図10-3)

塩基性の成分が含まれている？

二分葉の核 (HIS.197)
直径は10-14μm (HIS.197)
末梢血

顆粒

特殊顆粒とアズール顆粒をもつ (HIS.197)

アズール顆粒：水解酵素を含む

寄生虫の破壊、抗原抗体複合体の加水分解

特殊顆粒：主要塩基性タンパク質、好酸性陽イオンタンパク、好酸球由来神経毒素

アリルサルファターゼ、ヒスタミナーゼ、βグルクロニダーゼ、酸性ホスファターゼ、ホスホリパーゼ、主要塩基性蛋白、好酸性陽イオン蛋白、ニューロトキシン、リボヌクレアーゼ、カテプシン、ペルオキシダーゼ

機能 (HIS.198)

ケモカインによる遊走

ヒスタミン、ロイコトリエン、好酸球走化因子と結合して、これに向かって遊走する。

顆粒の分泌

主要塩基性タンパク、好酸性陽イオン、スーパーオキサイド、過酸化水素、ヒスタミン、ロイコトリエンCを放出
細胞毒を放出して寄生虫と戦う (HIS.107)
I型アレルギーにおける遅発型反応

抗原抗体複合体の取り込み、およびファゴサイト内での分解

抗原抗体複合体が存在すると結合組織の細胞がヒスタミンやIL-5を放出

基準値

好酸球比率(白血球比)：2-4%

好酸球数の変化

増加

寄生虫感染症、アレルギー疾患（特に、I型アレルギー）
喘息、ある種の腫瘍

減少：

腸チフス、パラチフス、副腎皮質ステロイド

サイトカイン

IL-5の受容→好酸球の前駆細胞増殖、前駆細胞から好酸球への分化促進 (HIS.197)

臨床関連

「造血幹細胞」

　　[★]

英: hematopoietic stem cell, HSC
関: 幹細胞

細胞表面マーカー

CD34
c-kit

分化

			血液中	組織
造血幹細胞 hematopoietic stem cell	リンパ球幹細胞 lymphoid stem cell	T細胞 T cell
		B細胞 B cell
		NK細胞 natuarl killer cell
	骨髄球幹細胞 myeloid stem cell	granulocyte/macrophage progenitor	好中球 neutrophil
			好酸球 eosinophil
			好塩基球 basophil
			unknown precursor of mast cell	肥満細胞 mast cell
			単球	マクロファージ macrophage
		赤芽球 erythroblast	赤血球 erythrocyte
		巨核球 megakaryocyte	血小板 platelet