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質問・ 解答例 PowerPoint PPT Presentation


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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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質問・ 解答例

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CD4T

Th1Th2

Th1Th2B

) CD8


CD4T

CD4T

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

Th1IFN

Th2IL-4/IL-5B

Th17IL-17

TregT


Th1Th2

MHCB

Th1Th2B

Th1IFN-CD40CD40

Th2IL-4, IL-5CD40BCD40L


) CD8

TMHCI

3BIDc


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


IL-12


IL-10

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

TMHCII

Th1NF-


IL-3, IL-5, GM-CSF

IL-2, IL-4, IL-7

IFN

TNF

TGF


IL-2, IL-4, IL-7


IL-3, IL-5, GM-CSF


IFN-IFN-

IFNAR: interferon alpha receptor1, 2

Tyrosine kinase 2


IFN-

IFNGR: interferon gamma receptor1, 2


JAK-STAT


JAKSTAT

Janus kinase; JAK

JAKSTAT

2STAT


TGF (transforming growth factor)

III

TGF

I

II


III

ISMADs

IITGF


67

BHL

B

B

T

B


HL

D-J

V-DJ

VDJ

VDJ

VDJ

mH

V-J

VJ

B

B

B

B

B

VDJ

mH, dH

VJ

B


Receptor editing:


IgMRAGL

clonal deletion)

B


BCXCR5CXCL13


B

BTTBT

TCXCR5TBBB


B

C

V (somatic hypermutation)Baffinity maturation)

BB


T

DNA

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

m(Sm)Sm


AID; activation-induced cytidine deaminase,

DNARNA


B

BBB

B2

2T


TI

BITAM

B

B


TIgM

2TIgG, IgA


TI

TIT

IgM


BITAM

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

IgMSrcBlk, Fyn, Lyn)IgITAM

SykIgITAMSykB


BB

MHCII-TBT2CD40L)

B


B

B(HEV)TTh2BTh2BTh2germinal center)


TB

T-MHCIITTCD40L


9

Fc


FcFc


Fc

IgGFcFcIgG

IgEFc


10

C3


IgMIgG

C3


C3b

C3b

C5a, C3a, C4a


C3

C4b2a(b)C3bBbC3C3C3aC3b

C3b

C3biC3b, C3dg, C3d

C3b iC3b + C3f C3dg + C3c C3d + C3g

C3b,iC3b,C3dg,C3d

CR1

CR2

C3a

CR3

CR4


TLR

NK/NKT


2

PRR, pattern recognition receptorTLRToll-like receptor

Toll(TLR)


CR1CR3CR4

2C3bCR1

C3bIiC3bCR3CR4

HIV

LDLLDL)


TLR


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.


(B7)T

CD4TTh1Th2


NK/NKT

FN-


NKMHC


TTCR (invariant)V14V8.2V7V2V24V11

-Galactosylceramide (-GalCer)


I


I

IgE,

IgEFcRI


1I

Th2T

Th2IL5

(EotaxinECF-A


Th2IgE

Th2


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