Allergen-stimulated T lymphocytes from allergic patients induce vascular cell adhesion molecule-1 (VCAM-1) expression and IL-6 production by endothelial cells.
Adhesion of inflammatory cells to endothelium is a critical step for their transvascular migration to inflammatory sites. To evaluate the relationship between T lymphocytes (TL) and vascular endothelium, supernatants from allergen-stimulated TL obtained from patients sensitive to Dermatophagoides pteronyssinus (Dpt) versus healthy subjects were added to endothelial cell (EC) cultures. TL were stimulated by autologous-activated antigen-presenting cells (APC) previously fixed in paraformaldehyde to prevent monokine secretion. Two parameters were measured: the expression of adhesion molecule and the production of IL-6. Related allergen-stimulated TL supernatants from allergic patients induced an increase of VCAM-1 and intercellular adhesion molecule-1 (ICAM-1) expression when supernatants of the control groups (TL exposed to an unrelated allergen or not stimulated or TL obtained from healthy subjects) did not. E-selectin expression was not modulated whatever the supernatant added to EC culture. IL-6 production by EC was significantly enhanced after activation with related allergen-stimulated TL supernatants from allergics compared with control supernatants. Induction of VCAM-1 expression was inhibited by adding neutralizing antibodies against IL-4, whereas IL-6 production and ICAM-1 expression were inhibited by anti-interferon-gamma (IFN-gamma) antibodies. Enhanced production of IL-4 and IFN-gamma was detected in related allergen-stimulated TL supernatants from allergic subjects compared with the different supernatants. These data suggest that allergen-specific TL present in the peripheral blood of allergic patients are of Th1 and Th2 subtypes. Their stimulation in allergic patients may lead to the activation of endothelial cells and thereby participate in leucocyte recruitment towards the inflammatory site.
Delneste
Y
Y
Unité INSERM U 416, Institut Pasteur, Lille, France.
Jeannin
P
P
Gosset
P
P
Lassalle
P
P
Cardot
E
E
Tillie-Leblond
I
I
Joseph
M
M
Pestel
J
J
Tonnel
A B
AB
D000328:Adult; D000485:Allergens / Q000276:immunology; D000938:Antigen-Presenting Cells / Q000276:immunology; D039741:Antigens, Dermatophagoides; D001180:Arthropod Venoms / Q000276:immunology; D001249:Asthma / Q000276:immunology; D015815:Cell Adhesion Molecules / Q000096:biosynthesis*; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000378:metabolism*; D006023:Glycoproteins / Q000276:immunology*; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology* / Q000473:pathology; D007371:Interferon-gamma / Q000502:physiology; D015847:Interleukin-4 / Q000502:physiology; D015850:Interleukin-6 / Q000096:biosynthesis*; D008875:Middle Aged; D011058:Pollen / Q000276:immunology; D012221:Rhinitis, Allergic, Perennial / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*; D019010:Vascular Cell Adhesion Molecule-1
D000485:Allergens; D039741:Antigens, Dermatophagoides; D001180:Arthropod Venoms; D015815:Cell Adhesion Molecules; D006023:Glycoproteins; D015850:Interleukin-6; D019010:Vascular Cell Adhesion Molecule-1; D015847:Interleukin-4; D007371:Interferon-gamma