Differential role of lymphocyte function-associated antigens in the activation of nickel-specific peripheral blood T lymphocytes.
The possible role(s) of the adhesion molecules LFA-1 alpha (CD11a), LFA-1 beta(CD18), ICAM-1 (CD54), CD2 (T11, LFA-2), and LFA-3 (CD58) in the in vitro activation of nickel-specific peripheral blood (PB) T lymphocytes was studied. For this purpose, monoclonal antibodies (MoAb) to these markers were used. Both LFA-2 and LFA-3 appeared to be consistently involved, whereas LFA-1 was inconsistently involved. In studies using antigen-presenting cells (APC) isolated from peripheral blood to present nickel, anti-LFA-1 alpha and/or LFA-1 beta MoAb partially inhibited the in vitro activation of nickel-specific T lymphocytes in nine of 42 patients allergic to nickel. In the other 33 patients variable results, ranging from a slight increase or inhibition of proliferation to no inhibition at all, was observed, in particular when different anti-LFA-1 alpha MoAb were added to the cultures. In those patients who showed no inhibition when anti-LFA-1 (alpha and beta) MoAb were added, no inhibition was also observed when a mixture of anti-LFA-1 (alpha and beta) and ICAM-1 MoAb were added to the cultures. Similar results were also obtained using epidermal APC. In control experiments the various anti-LFA-1 (alpha and beta) MoAb effectively inhibited the tetanus toxoid and Con-A induced T-lymphocyte proliferation as well as the spontaneous aggregation of the JY cell line. Anti-CD2 and anti-LFA-3 MoAb strongly inhibited the proliferative responses of nickel-specific peripheral blood T lymphocytes from all 42 patients. These results indicated that the receptor-ligand interaction between CD2 and LFA-3 is essential for in vitro activation of nickel-specific peripheral blood T lymphocytes. This activation, however, does not regularly involve LFA-1 molecules on T lymphocytes. The involvement of LFA-1 in the activation of nickel-specific T lymphocytes correlated positively with high patch test scores to nickel and the disease activity in contact dermatitis patients.
Department of Dermatology, University Hospital Rotterdam-Dijkzigt and Erasmus University, The Netherlands.
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Prens
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Benne
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van Joost
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Benner
D000293:Adolescent; D000328:Adult; D000911:Antibodies, Monoclonal; D000938:Antigen-Presenting Cells / Q000276:immunology; D015815:Cell Adhesion Molecules / Q000502:physiology*; D003877:Dermatitis, Contact / Q000276:immunology; D006801:Humans; D016130:Immunophenotyping; D008213:Lymphocyte Activation / Q000187:drug effects*; D016169:Lymphocyte Function-Associated Antigen-1 / Q000502:physiology*; D008274:Magnesium / Q000494:pharmacology; D008875:Middle Aged; D009532:Nickel / Q000276:immunology*; D016176:T-Lymphocyte Subsets / Q000276:immunology*
D000911:Antibodies, Monoclonal; D015815:Cell Adhesion Molecules; D016169:Lymphocyte Function-Associated Antigen-1; D009532:Nickel; D008274:Magnesium