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質問・ 解答例. 講義1,2. 1) CD4 陽性 T 細胞は4種類のエフェクター細胞へ分化するが、それは何が決めているのか? 2)また、 4種類のエフェクター細胞の機能は何でしょうか? . 3) Th1 或いは Th2 細胞を、どのような細胞を認識し、活性化するのか?. 4) Th1 或いは Th2 細胞は、マクロファージ或いは B 細胞をどのように活性化するでしょか?. 5 ) CD8 陽性キラー細胞はどのような機構で細胞を殺傷しているのでしょうか?. 1) CD4 陽性 T 細胞は4種類のエフェクター細胞へ分化するが、それは何が決めているのか?

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3877190


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CD4T

Th1Th2

Th1Th2B

) CD8


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CD4T

CD4T

IL-12/IFNTh1IL-4Th2TGF+IL-6Th17TGFTreg

Th1IFN

Th2IL-4/IL-5B

Th17IL-17

TregT


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Th1Th2

MHCB

Th1Th2B

Th1IFN-CD40CD40

Th2IL-4, IL-5CD40BCD40L


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) CD8

TMHCI

3BIDc


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IL-1~7,1012 IFNTNFLTsTGFGM- C- M-CSF


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IL-12


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IL-10

IL-1IL-6Il-12TNF-CD80CD86

TMHCII

Th1NF-


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IL-3, IL-5, GM-CSF

IL-2, IL-4, IL-7

IFN

TNF

TGF


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IL-2, IL-4, IL-7


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IL-3, IL-5, GM-CSF


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IFN-IFN-

IFNAR: interferon alpha receptor1, 2

Tyrosine kinase 2


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IFN-

IFNGR: interferon gamma receptor1, 2


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JAK-STAT


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JAKSTAT

Janus kinase; JAK

JAKSTAT

2STAT


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TGF (transforming growth factor)

III

TGF

I

II


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III

ISMADs

IITGF


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67

BHL

B

B

T

B


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HL

D-J

V-DJ

VDJ

VDJ

VDJ

mH

V-J

VJ

B

B

B

B

B

VDJ

mH, dH

VJ

B


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Receptor editing:


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IgMRAGL

clonal deletion)

B


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BCXCR5CXCL13


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B

BTTBT

TCXCR5TBBB


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B

C

V (somatic hypermutation)Baffinity maturation)

BB


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T

DNA

HC(Cm, Cd, Cg3, Cg1,Ca1,Cg2, Cg4, Ce, Ca2)DNASSDNAIgM, IgD

m(Sm)Sm


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AID; activation-induced cytidine deaminase,

DNARNA


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B

BBB

B2

2T


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TI

BITAM

B

B


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TIgM

2TIgG, IgA


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TI

TIT

IgM


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BITAM

ITAMD/E)X 7(D/E)X2(Y)X2(L/I)X7(Y)X2(L/I) Ig, Ig

IgMSrcBlk, Fyn, Lyn)IgITAM

SykIgITAMSykB


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BB

MHCII-TBT2CD40L)

B


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B

B(HEV)TTh2BTh2BTh2germinal center)


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TB

T-MHCIITTCD40L


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9

Fc


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FcFc


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Fc

IgGFcFcIgG

IgEFc


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10

C3


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IgMIgG

C3


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C3b

C3b

C5a, C3a, C4a


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C3

C4b2a(b)C3bBbC3C3C3aC3b

C3b

C3biC3b, C3dg, C3d

C3b iC3b + C3f C3dg + C3c C3d + C3g

C3b,iC3b,C3dg,C3d

CR1

CR2

C3a

CR3

CR4


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TLR

NK/NKT


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2

PRR, pattern recognition receptorTLRToll-like receptor

Toll(TLR)


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CR1CR3CR4

2C3bCR1

C3bIiC3bCR3CR4

HIV

LDLLDL)


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TLR


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Nature Immunology, 2011

TLR4 signaling activates the canonical IKK complex via MyD88-dependent and TRIF-dependent mechanisms. MyD88 assembles complexes that contain IRAK kinases together with TRAF6, TAB2, TAB3 and TAK1. TRIF can directly recruit TRAF6 and recruit TAB2, TAB3 and TAK1. The active NF-B pathway subsequently induces expression of the alternative MyD88 splice product MyD88s, the kinase-inactive IRAK family member IRAK-M and the negative regulatory adaptor molecule SARM. These dominant-negative factors presumably affect the stability of the IKK-activating complexes.


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(B7)T

CD4TTh1Th2


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NK/NKT

FN-


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NKMHC


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TTCR (invariant)V14V8.2V7V2V24V11

-Galactosylceramide (-GalCer)


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I


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I

IgE,

IgEFcRI


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1I

Th2T

Th2IL5

(EotaxinECF-A


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Th2IgE

Th2


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