. , , ,

,,,

. —

 2

/ - /

- ,

, . /2300/96/

 2 :

 11. ( = - ) 0,

-1 HLA I.

-

- -

- //

-

-

-

 12.

- - (- -)

- (-) (-) - -

, ;

- s (-) _ , ;

/s - 2,0-2,5;

- -

- - ( )

- -

- -

 13.

- = (-) ── 76 0

- (-)

(-, -, - -

- FcR;

- )

.

 _ 2K-, NK-,-, L- 0 (5-10% )

. -

.

3 .

-, L- -

-

, NK - . /7072/

───────────────────────────────────────────────────────────────

0- │ -

───────────────────────────────────────────────────────────────

(

)

- ── 76 0 -֠

L- ── 76 0 -֠ -

───────────────────────────────────────────────────────────────

.

 2 0 - . " "

 2

, (, ,

) --

.

-

- -  2 0 -

(, -

, - -

, );

- - 2  0(,

-

, ).

/7284/90/

───────────────────────────────────────────────────────────────

蠠 │ (=), │ 1  0── 76 0

───────────────────────────────────────────────────────────────

/ :

Ƞ  2CR1 0 (30000 ) 3/4 ── 76 0

CR2, 3d - " - ?

R3 3i ( )

C5R 5 (

) /7683/

 2Fc 7g 2R 0 ʠ ── 76 0

 2- - 0 , . ── 76

 2 0

/

R  7 0- (6-8 .)

-1)

R

R ,

R Pg E2

R (/)

: CD11,; D12,

CD14; HLA II, Mo,

Mac1-3 (=HLA A2)

/6504/

 7 0v 7b 03- (

)

── 76 0

FasR FasL (, -

 5 FasL-FasR

 5젠 --R,

 5CD40L-CD40,

 5--R ( ). /2333/

-۠ CD2 R -

(-)

(Fc 7m 0R,Fc 7g 0R,Fc 7a 0R,Fc 7e 0R - ?)

젠  2  0── 76 2

7000 .

Ig -? /7662/

:

3 + i + CD3 R

-۠

-  2R1 0 (2000 -?) 3,4,5 (-)── 76

- ?

- CR2 ( - 3d (

. - )

,,

.

.)

 21qR  0 1q ── 76 0

 2Fc 7 2R 0-? 2Fc 7 2R,Fc 7 2R,Fc 7e 2R 7  0 ── 76 0

(-)

 2 Ig  0───┬─────── + ── 76 0 .

└─────── + ── 76

-

 _ . : Ge,U, Jk 3,

Yt a, HLA, NA 1,2,

NB1, NC1, ND1

(N-,A-D-

,1-4-).

:

 2Fc 7g 2R,Fc 7a 2R  0 ── 76 0

3/ 2C5aR 0 (40-300 5 ── 76 0

)

 2CR1 0 - 20000  2 3/4  0── 76 2

CR2, 3d

R3 3i

 _ . :

Fc 7g 0R ── 76 0 ? (,)

Fc 7e 0R-? -- ()

3R,C5aR

R1,CR3

 _ . :

Fc 7g 0R

 2Fc 7e 2R 0 -- ()

,

3/ 2C5aR 0 5 ── 76 0 ── 76 0 -

── 76 0

:

- " - ,

(Fc 7g 0R, 2Fc 7e 2R 0 (.Ig + )

3R, 2C5aR 0) 3,5,

۠ :

1qR 1q ── 76 0

Fc 7g 0R ── 76 0 -?

: , , i, , ,

Lek, PL, Bd-3, Ko 5a,b 0, , ,

k,Zw 5a,b 0

Ƞ R -1, ...

+ Ѡ

:

FcR ʠ ─ 76 0 (=

?)

( .)

1qR /?/

5R

/?/ ...

:

 _ = -

PAL - (

-

)

ʠ R3 /1R1094-94-Bv-z/

 4 C1q, C3a,

 44a C5a. 3b 3

 4 , ,

 4 Fc- ,

 4 3

 4. C1q,

 4, (). ,

 4-, -

 4 C1q (cc).

 4 -

 4 , IIa .

 4 , -

 4 ,

 45b-C9. -

 4, , ,

 4 3-,

 4 5b-9,

 4 .

 4 .

۠ : (),Rh (),

MNS, Kk, Fy (), Lu

(), Le ()

:

 2R1  0( 3) - 500 ࠠ 3 ── 76 0

󠠠

Ƞ :

Fc 7e 0R /7610/

───────────────────────────────────────────────────────────────

 1───────────────────────────────────────────────────────────────

 1

 1ʠ

 1

 1

 1( )

 1

 1

 1ʠ ,. Staph.,-S

 1 (+-), .II,

 1 ,

 1

 1ʠ ., (- -

 1), ,

 1───────────────────────────────────────────────────────────────

.

...

.

───────────────────────────────────────────────────────────────

, │ │ ── 76 0

───────────────────────────────────────────────────────────────

:

 21qR  0 1q - ── 76 0

── 76 0

 2CR1 0, 3/4⠠ ── 76 0

- ── 76 0 - ?

(-=-)

── 76 0

── 76 0

CR2, 3d ── 76 0 ?

-── 76 0

── 76

R3 3i ─── 76 0 ?

── 76

C5R 5/3ࠠ ── 76 0 ?

── 76 0

,

FcR

 2Fc 7 2R 0-? 2Fc 7 2R,Fc 7 2R,Fc 7e 2R 7  0

ʠ - ── 76 0

(-)

 2Fc 7g 2R 0 ʠ ── 76 0

 2 Ig  0─┬ +à - ── 76 0 (

│ - )

└ +-

Ҡ ── 76 0 -

 2-

 2  0 . Ѡ ── 76 0

젠 - ── 76 0

Fc 7m 0R- ?

Fc 7g 0R ʠ ── 76 0

,

── 76 0 /?/

Fc 7a 0R ʠ ── 76 0

Fc 7e 0R+Ig E à

── 76 0 (

)

── 76 0 - " -

───────────────────────────────────────────────────────────────

/7272/95-./

2 : Ig (Ig--

) R. .

R -1 -1

(.R-?)

Ig - ?

- ࠠ -

.

- ࠠ -

-?

R -2 -2 - -

(.R) -?

R -3 -3

(.R)

R -4 -4 - -

(.R)

R -5 -5 ,

(.R)

R -6 -6 -,

(.R)

R -7 -7 -,

(.R)

𠠠 ,

,

R -8 -8 ,

-,

( R 7 砠 ,

򠠠

,

)

───────────────────────────────────────────────────────────────

.

Hargreaves RG. Borthwick NJ. Montani MS. Piccolella E. Carmichael P.

Lechler RI. Akbar AN. Lombardi G.

Dissociation of T cell anergy from  _apoptosis by blockade of Fas/Apo-1

(CD95) signaling.

Journal of Immunology. 158(7):3099-107, 1997 Apr 1.

Induction of anergy and deletion due to apoptosis are two of the

mechanisms involved in peripheral tolerance. To clarify the relationship

between these two phenomena we have used an in vitro system of T cell Ag

presentation. The recognition of Ag displayed by MHC class II-expressing T

cells (T-APC) induces partial signals in Ag-specific T cell clones. This

leads to a blunted intracellular calcium flux, and the T cells become

unable to proliferate in response to further challenge with professional

APC. These T cells are unable to produce IL-2, but retain the ability to

release IL-4. In the present study, we report that for some T cell clones,

the predominant outcome of Ag recognition on T cells is cell death. For

susceptible T cell clones, the number of cells that die is proportional to

the peptide concentration. This cell death resulted from Fas/Apo-1

(CD95)/Fas-ligand interactions between the T cells, in that Fas ligand

expression was detected following overnight culture of T cells with T-APC

and neutralizing anti-CD95 Ab protected from death. Most notably,

following anti-CD95-mediated protection from apoptosis, the rescued T

cells remained unable to respond to rechallenge with Ag-pulsed,

professional APC. These data suggest that anergy and apoptosis can be

separated as consequences of partial T cell signaling.

Weismann M. Guse AH. Sorokin L. Broker B. Frieser M. Hallmann R.

Mayr GW.

Integrin-mediated intracellular Ca2+ signaling in Jurkat T lymphocytes.

Journal of Immunology. 158(4):1618-27, 1997 Feb 15.

T lymphocytes interact with components of the extracellular matrix after

transendothelial migration on their way to sites of inflammation. To

characterize the molecular basis of the interaction between T lymphocytes

with different extracellular matrix proteins, we investigated the role of

intracellular Ca2+ as a signal mediating such interactions and identified

the cell surface integrins involved in this process. When Jurkat T

lymphocytes loaded with the calcium-sensitive fluorescent dye fura-2 were

placed on coverslips coated with human fibronectin, human collagen types

I, IV, and VI, human tenascin, human laminin I, or mouse laminin I, an

elevation in intracellular Ca2+ concentration was observed. In contrast,

contact of the Jurkat T lymphocytes with vitronectin and thrombospondin

did not induce Ca2+ signals in more cells as compared with control

measurements in which cells were in contact with only BSA or polylysine.

Furthermore, the percentage of Jurkat T lymphocytes responding with Ca2+

signals to collagen types I and IV, fibronectin, and laminin I was

completely reduced to levels observed on BSA or polylysine when the cells

were pretreated with specific anti-integrin Abs, suggesting a role for

cell surface integrins as mediators of cell matrix-induced intracellular

Ca2+ signaling. Similar results were obtained with peripheral human T

lymphocytes activated by phytohemagglutinin.

2 / - / - , , . /2300/96/ 2 :

 

 

 

! , , , .
. , :