Anti-lymphocyte function associated antigen-1 inhibits T-helper 2 function of human allergen-specific CD4+ T cells
Ardern-Jones, M.R., Black, A.P. and Ogg, G.S. (2008) Anti-lymphocyte function associated antigen-1 inhibits T-helper 2 function of human allergen-specific CD4+ T cells. British Journal of Dermatology, 158, (3), 456-462. (doi:10.1111/j.1365-2133.2007.08393.x). (PMID:18205875).
Full text not available from this repository.
Background: Blockade of lymphocyte function associated antigen-1 (LFA-1) is proving successful in the management of psoriasis and other inflammatory skin conditions including atopic dermatitis (AD), but the dependence of allergen-specific CD4+ T-cell function on LFA-1 has not been studied extensively.
Objectives: We sought to investigate the potential ability of LFA-1 inhibition to influence keratinocyte presentation of allergen to specific T-helper (Th) 2 cell clones.
Methods: Using human leucocyte antigen class II tetrameric complexes, we generated Der p 1-specific DRB1*1501-restricted CD4+ T-cell lines (n = 5) and clones (n = 4) from the peripheral blood of five adults with AD.
Results: Using doses of anti-LFA-1 present in vivo, we observed significant inhibition (P < 0·05) of allergen-specific CD4+ T-cell production of interleukin-4 with such inhibition occurring during presentation of allergen by keratinocytes.
Conclusions: These data show that at doses present in vivo, LFA-1 blockade inhibits keratinocyte presentation to allergen-specific Th2 cells, suggesting one mechanism through which anti-LFA-1 may be beneficial therapeutically.
|Digital Object Identifier (DOI):||doi:10.1111/j.1365-2133.2007.08393.x|
|Keywords:||atopic dermatitis, t cells|
|Subjects:||Q Science > QR Microbiology > QR180 Immunology
R Medicine > RL Dermatology
|Divisions:||University Structure - Pre August 2011 > School of Medicine > Infection, Inflammation and Repair
|Date Deposited:||18 Apr 2011 14:28|
|Last Modified:||27 Mar 2014 19:34|
|RDF:||RDF+N-Triples, RDF+N3, RDF+XML, Browse.|
Actions (login required)