Table S1.

CCR8 Expression in Human T Cell Clones Derived from Various Skin Lesions

Clone

CD4

CD8

CCR8

CCR4

CCR6

Pustular psoriasis

VK S3

100a

 

0b

10c

10

VK S5

100

 

8

24

100

VK S8

100

 

100

VK S9

100

 

7

100

VK S13

100

 

9

100

VK S14

100

 

7

100

VK S15

 

100

90

VK S18

 

100

18

VK S24

 

100

9

6

92

VK S26

100

 

8

37

VK S40

100

 

29

91

VK S50

100

 

12

94

Acute generalized exanthematous pustulosis

AP S38

100

 

100

AP S46

100

 

100

UlSt S1

100

 

42

29

100

UlSt S4

100

 

7

100

UlSt S6

100

 

68

6

100

UlSt S7

100

 

8

100

UlSt S8

100

 

6

100

UlSt S9

100

 

9

100

UlSt S10

100

 

94

UlSt S11

100

 

7

93

UlSt S15

100

 

47

UlSt S16

100

 

6

8

33

UlSt S30

100

 

100

Behcet’s disease

DP S5

100

 

8

91

DP S10

100

 

29

10

DP S17.2

100

 

100

DP S20

100

 

28

100

DP S25

100

 

15

96

DP S33

100

 

33

74

DP S34

100

 

24

20

DP S35

100

 

67

55

DP S49

100

 

48

11

34

DP S50

100

 

9

DP S54

100

 

21

100

DP S66

100

 

13

aIndicates >95% of positive cells determined by flow cytometry. bIndicates <5% of positive cells determined by flow cytometry. cA low but homogenous staining was observed, which suggests that numbers indicated may underestimate the real positive CCR4 fraction.

The migration properties of T cell clones derived from various human skin diseases. This work was undertaken to determine the extent of CCR8 positivity among T cells present at inflammatory skin lesions. It is known that effector T cells with selectivity for inflammatory chemokines predominate at inflammatory sites. Here, we analyzed a total of 37 human T cell clones derived from diverse skin lesions for expression of CCR8 as well as CCR4 and CCR6. Four clones expressed medium to high levels of CCR8, whereas 13 and 35 clones were highly positive for CCR4 and CCR6, respectively. We conclude that CCR8- T cells do not predominate at inflammatory skin lesions, which agrees with the homeostatic as opposed to inflammatory regulation of its ligand CCL1.

Disease