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Major histocompatibility complex class I‐restricted alloreactive CD4 + T cells
Author(s) -
Boyle Louise H.,
Goodall Jane C.,
Gaston J. S. Hill
Publication year - 2004
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2004.01857.x
Subject(s) - major histocompatibility complex , mhc restriction , biology , human leukocyte antigen , mhc class i , mhc class ii , transporter associated with antigen processing , monoclonal antibody , cd1 , antigen , cd74 , immunology , antigen processing , t cell , cd8 , microbiology and biotechnology , antibody , immune system , natural killer t cell
Summary Although it is well established that CD4 + T cells generally recognize major histocompatibility complex (MHC) class II molecules, MHC class I‐reactive CD4 + T cells have occasionally been reported. Here we describe the isolation and characterization of six MHC class I‐reactive CD4 + T‐cell lines, obtained by co‐culture of CD4 + peripheral blood T cells with the MHC class II‐negative, transporter associated with antigen processing (TAP)‐negative cell line, T2, transfected with human leucocyte antigen (HLA)‐B27. Responses were inhibited by the MHC class I‐specific monoclonal antibody (mAb), W6/32, demonstrating the direct recognition of MHC class I molecules. In four cases, the restriction element was positively identified as HLA‐A2, as responses by these clones were completely inhibited by MA2.1, an HLA‐A2‐specific mAb. Interestingly, three of the CD4 + T‐cell lines only responded to cells expressing HLA‐B27, irrespective of their restricting allele, implicating HLA‐B27 as a possible source of peptides presented by the stimulatory MHC class I alleles. In addition, these CD4 +  MHC class I alloreactive T‐cell lines could recognize TAP‐deficient cells and therefore may have particular clinical relevance to situations where the expression of TAP molecules is decreased, such as viral infection and transformation of cells.

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