The interleukin-13 production by peripheral blood T cells from atopic dermatitis patients does not require CD2 costimulation.
BACKGROUND
Although allergic mechanisms appear to be important, the pathogenesis of both extrinsic and intrinsic forms of atopic dermatitis (AD) is unknown.


METHODS
We compared the cytokine production of peripheral blood mononuclear cells of extrinsic AD (EAD) and intrinsic AD (IAD) patients and normal control individuals after stimulation with anti-CD3 and/or anti-CD28 monoclonal antibodies (mAbs) in the presence or absence of anti-CD2-blocking mAb. The cytokine production was measured by immunoassays in supernatants of 24-hour cultures.


RESULTS
EAD patients showed a decreased capacity to synthesize interferon gamma and granulocyte-macrophage colony-stimulating factor upon anti-CD3 mAb stimulation as compared with IAD patients. Both EAD and IAD patients demonstrated an increased production of interleukin (IL)-5 and IL-13. As expected, interferon gamma, granulocyte-macrophage colony-stimulating factor, and IL-5 levels were reduced in the presence of anti-CD2-blocking mAbs. CD28 costimulation restored the release in cultures with anti-CD2 mAbs added, suggesting that CD2 and CD28 have redundant functions in T cell activation and subsequent cytokine production. Strikingly, the IL-13 production was not blocked by anti-CD2 mAbs and also not increased by agonistic anti-CD28 mAb, in particular within the EAD patient group.


CONCLUSIONS
The signalling pathway initiated by the T cell receptor complex leading to increased IL-13 production in AD patients appears to be highly sensitive and is largely independent on CD2 costimulatory signals.
Department of Dermatology, University of Bern, Bern, Switzerland. dagmar.simon@insel.ch
Dagmar
D
Simon
Stephan
S
Von Gunten
Siegfried
S
Borelli
Lasse R
LR
Braathen
Hans-Uwe
HU
Simon
D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000276:immunology; D018801:CD2 Antigens / Q000276:immunology* / Q000378:metabolism; D018106:CD28 Antigens; D002455:Cell Division / Q000276:immunology; D003876:Dermatitis, Atopic / Q000276:immunology* / Q000378:metabolism; D005260:Female; D006801:Humans; D018793:Interleukin-13 / Q000096:biosynthesis* / Q000276:immunology; D008213:Lymphocyte Activation / Q000276:immunology; D008297:Male; D008875:Middle Aged; D013601:T-Lymphocytes / Q000276:immunology* / Q000378:metabolism
D000911:Antibodies, Monoclonal; D018801:CD2 Antigens; D018106:CD28 Antigens; D018793:Interleukin-13